General Information of the Disease (ID: M6ADIS0070)
Name
Bladder cancer
ICD
ICD-11: 2C94
Full List of Target Gene(s) of This m6A-centered Disease Response
AF4/FMR2 family member 4 (AFF4)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Glucose metabolism
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [2]
Response Summary METTL3 regulates the m6A modification and thereby the expression of AF4/FMR2 family member 4 (AFF4), knockdown of which phenocopies the METTL3 ablation and diminishes the tumor-initiating capability of bladder cancer stem cells in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response Signaling pathways regulating pluripotency of stem cells hsa04550
Cell Process Self-renewal and tumorigenicity
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
Angiopoietin-1 receptor (TEK)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [3]
Response Summary Deletion of Mettl3 leads to the suppression of Angiopoietin-1 receptor (TEK) and VEGF-A,ablation of Mettl3 in bladder urothelial attenuates the oncogenesis and tumor angiogenesis of bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cellular proliferation and survival
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
In-vivo Model For induction of BCa, 6-8-week-old mice were treated with drinking water containing 500 ug/ml BBN for 16 weeks and then given normal water for another 10 weeks. Tamoxifen was intraperitonelly injected to the mice with 0.08 mg/g of body weight each day for 3 days in order to inductively knock out the target gene.
Casein kinase II subunit alpha' (CSNK2A2)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [4]
Response Summary knockdown of ALKBH5 promoted bladder cancer cell proliferation, migration, invasion, and decreased cisplatin chemosensitivity, ALKBH5 inhibited the progression and sensitized bladder cancer cells to cisplatin through a Casein kinase II subunit alpha' (CSNK2A2)-mediated glycolysis pathway in an m6A-dependent manner.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Cisplatin Approved
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Down regulation
Pathway Response Metabolic pathways hsa01100
Glycolysis / Gluconeogenesis hsa00010)
Cell Process Glycolysis
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
J82 Bladder carcinoma Homo sapiens CVCL_0359
253J Bladder carcinoma Homo sapiens CVCL_7935
5637 Bladder carcinoma Homo sapiens CVCL_0126
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [5]
Response Summary In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of Casein kinase II subunit alpha' (CSNK2A2) and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Pathway Response Notch signaling pathway hsa04330
Cell Process Cell proliferation
Cell invasion
Cell apoptosis
In-vitro Model HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
In-vivo Model BALB/cnu/nu mice (4-5 weeks old) were used for the xenograft experiment. The mice were randomly divided into 2 groups (n = 6 for each group) and injected with 5 × 106 HT-1197 cells in control group or FTO plasmid group, respectively.
CUB domain-containing protein 1 (CDCP1)
In total 3 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [6]
Response Summary m6A methyltransferase METTL3 and demethylases ALKBH5 mediate the m6A modification in 3'-UTR of CDCP1 mRNA. METTL3 and CUB domain-containing protein 1 (CDCP1) are upregulated in the bladder cancer patient samples and the expression of METTL3 and CDCP1 is correlated with the progression status of the bladder cancers.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
RWPE-1 Normal Homo sapiens CVCL_3791
NSTC2 (Nickel-induced transformation of human cells)
MC-SV-HUC T-2 Ureteral tumor cell Homo sapiens CVCL_6418
16HBE14o- Normal Homo sapiens CVCL_0112
In-vivo Model To test for malignant transformation, 1×107 cells were inoculated subcutaneously in the dorsal thoracic midline of ten NOD/SCID mice (Weitong Lihua Experimental Animal Technology Co. Ltd). Tumor formation and growth were assessed every 3 days.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [6]
Response Summary m6A methyltransferase METTL3 and demethylases ALKBH5 mediate the m6A modification in 3'-UTR of CDCP1 mRNA. METTL3 and CUB domain-containing protein 1 (CDCP1) are upregulated in the bladder cancer patient samples and the expression of METTL3 and CDCP1 is correlated with the progression status of the bladder cancers.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Down regulation
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
RWPE-1 Normal Homo sapiens CVCL_3791
NSTC2 (Nickel-induced transformation of human cells)
MC-SV-HUC T-2 Ureteral tumor cell Homo sapiens CVCL_6418
16HBE14o- Normal Homo sapiens CVCL_0112
In-vivo Model To test for malignant transformation, 1×107 cells were inoculated subcutaneously in the dorsal thoracic midline of ten NOD/SCID mice (Weitong Lihua Experimental Animal Technology Co. Ltd). Tumor formation and growth were assessed every 3 days.
Experiment 3 Reporting the m6A-centered Disease Response by This Target Gene [7]
Response Summary The RCas9-METTL3 system mediates efficient sitespecific m6A installation on CUB domain-containing protein 1 (CDCP1) mRNA and promotes bladder cancer development.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
Cyclin-dependent kinase 6 (CDK6)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [8]
Response Summary FTO promoted bladder cancer cell proliferation, migration and invasion via the FTO/miR-576/Cyclin-dependent kinase 6 (CDK6) pathways in an m6A-dependent manner.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model Approximately 1 × 107 stably transfected T24 cells were subcutaneously injected into BALB/c nude mice. The length (L) and width (W) of the tumours were measured weekly using callipers, while their volume was calculated using the equation: V = (L × W2)/2. After 4 weeks of injections, the mice were euthanised, and the tumour tissues were removed and weighed.
Histone-lysine N-methyltransferase SETD7 (SETD7)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [9]
Response Summary METTL3/YTHDF2/Histone-lysine N-methyltransferase SETD7 (SETD7)/KLF4 m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Down regulation
Cell Process Cancer proliferation
Cancer metastasis
In-vitro Model SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, UM-UC-3 cells (2 × 106 cells per mouse) stably METTL3 knocked down (shMETTL3-1, shMETTL3-2) were injected into the flanks of mice.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [9]
Response Summary METTL3/YTHDF2/Histone-lysine N-methyltransferase SETD7 (SETD7)/KLF4 m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process Cancer proliferation
Cancer metastasis
In-vitro Model SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, UM-UC-3 cells (2 × 106 cells per mouse) stably METTL3 knocked down (shMETTL3-1, shMETTL3-2) were injected into the flanks of mice.
Inhibitor of nuclear factor kappa-B kinase subunit beta (IKBKB)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (Inhibitor of nuclear factor kappa-B kinase subunit beta (IKBKB) and RELA) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Glucose metabolism
Integrin alpha-6 (ITGA6)
In total 5 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [10]
Response Summary m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response Cell adhesion molecules hsa04514
Cell Process Cell adhesion
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
HEK293T Normal Homo sapiens CVCL_0063
J82 Bladder carcinoma Homo sapiens CVCL_0359
SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, 1 × 107 cells were subcutaneously implanted into 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [10]
Response Summary m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Pathway Response Cell adhesion molecules hsa04514
Cell Process Cell adhesion
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
HEK293T Normal Homo sapiens CVCL_0063
J82 Bladder carcinoma Homo sapiens CVCL_0359
SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, 1 × 107 cells were subcutaneously implanted into 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice.
Experiment 3 Reporting the m6A-centered Disease Response by This Target Gene [10]
Response Summary m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator YTH domain-containing family protein 1 (YTHDF1) READER
Pathway Response Cell adhesion molecules hsa04514
Cell Process Cell adhesion
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
HEK293T Normal Homo sapiens CVCL_0063
J82 Bladder carcinoma Homo sapiens CVCL_0359
SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, 1 × 107 cells were subcutaneously implanted into 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice.
Experiment 4 Reporting the m6A-centered Disease Response by This Target Gene [10]
Response Summary m6A writer METTL3 and eraser ALKBH5 altered cell adhesion by regulating Integrin alpha-6 (ITGA6) expression in bladder cancer cells. m6A is highly enriched within the ITGA6 transcripts, and increased m6A methylations of the ITGA6 mRNA 3'UTR promotes the translation of ITGA6 mRNA via binding of the m6A readers YTHDF1 and YTHDF3. Inhibition of ITGA6 results in decreased growth and progression of bladder cancer cells in vitro and in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator YTH domain-containing family protein 3 (YTHDF3) READER
Pathway Response Cell adhesion molecules hsa04514
Cell Process Cell adhesion
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
HEK293T Normal Homo sapiens CVCL_0063
J82 Bladder carcinoma Homo sapiens CVCL_0359
SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, 1 × 107 cells were subcutaneously implanted into 5-week-old BALB/cJNju-Foxn1nu/Nju nude mice.
Experiment 5 Reporting the m6A-centered Disease Response by This Target Gene [5]
Response Summary In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and Integrin alpha-6 (ITGA6) transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Pathway Response Notch signaling pathway hsa04330
Cell Process Cell proliferation
Cell invasion
Cell apoptosis
In-vitro Model HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
In-vivo Model BALB/cnu/nu mice (4-5 weeks old) were used for the xenograft experiment. The mice were randomly divided into 2 groups (n = 6 for each group) and injected with 5 × 106 HT-1197 cells in control group or FTO plasmid group, respectively.
Krueppel-like factor 4 (KLF4)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [9]
Response Summary METTL3/YTHDF2/SETD7/Krueppel-like factor 4 (KLF4) m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Down regulation
Cell Process Cancer proliferation
Cancer metastasis
In-vitro Model SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, UM-UC-3 cells (2 × 106 cells per mouse) stably METTL3 knocked down (shMETTL3-1, shMETTL3-2) were injected into the flanks of mice.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [9]
Response Summary METTL3/YTHDF2/SETD7/Krueppel-like factor 4 (KLF4) m6 A axis provide the insight into the underlying mechanism of carcinogenesis and highlight potential therapeutic targets for bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process Cancer proliferation
Cancer metastasis
In-vitro Model SV-HUC-1 Normal Homo sapiens CVCL_3798
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model For the subcutaneous implantation model, UM-UC-3 cells (2 × 106 cells per mouse) stably METTL3 knocked down (shMETTL3-1, shMETTL3-2) were injected into the flanks of mice.
Myc proto-oncogene protein (MYC)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and RELA) and Myc proto-oncogene protein (MYC) were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Glucose metabolism
Neurogenic locus notch homolog protein 1 (NOTCH1)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [11]
Response Summary Mettl14 and m6A modification participate in the RNA stability of Neurogenic locus notch homolog protein 1 (NOTCH1) mRNA. Notch1 plays an essential role in bladder tumorigenesis and bladder TIC self-renewal.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Cell Process Cell proliferation
Self-renewal
Cell metastasis
In-vitro Model Primary bladder cancer cells (Obtained from bladder cancer patients)
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [5]
Response Summary In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and Neurogenic locus notch homolog protein 1 (NOTCH1) transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Down regulation
Pathway Response Notch signaling pathway hsa04330
Cell Process Cell proliferation
Cell invasion
Cell apoptosis
In-vitro Model HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
In-vivo Model BALB/cnu/nu mice (4-5 weeks old) were used for the xenograft experiment. The mice were randomly divided into 2 groups (n = 6 for each group) and injected with 5 × 106 HT-1197 cells in control group or FTO plasmid group, respectively.
Neurogenic locus notch homolog protein 2 (NOTCH2)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [12]
Response Summary METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/miR-146a-5p/NUMB/Neurogenic locus notch homolog protein 2 (NOTCH2) axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Melittin Investigative
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process miRNA maturation
Cell apoptosis
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
EJ (Human bladder cancer cells)
BIU-87 Human bladder cancer cells Homo sapiens CVCL_6881
In-vivo Model For melittin treatment study, 4-week-old female BALB/c nude mice were subcutaneously injected with 1 × 107 T24 or BIU87 cells.
P5C reductase 1 (PYCR1)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [13]
Response Summary FTO decreased N6-methyladenosine methylation level in P5C reductase 1 (PYCR1) through its demethylase enzymatic activity and stabilized PYCR1 transcript to promote bladder cancer initiation and progression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Pathway Response mRNA surveillance pathway hsa03015
RNA degradation hsa03018
Cell Process RNA stability
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
RT-4 Bladder carcinoma Homo sapiens CVCL_0036
J82 Bladder carcinoma Homo sapiens CVCL_0359
EJ (Human bladder cancer cells)
5637 Bladder carcinoma Homo sapiens CVCL_0126
In-vivo Model T24 cells were subcutaneously injected into the mice (1 x 106 cells / injecting site).
Programmed cell death 1 ligand 1 (CD274/PD-L1)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [14]
Response Summary m6A-related prognostic lncRNA signature serves as a crucial mediator of the immune microenvironment in bladder cancer, representing promising therapeutic targets for improving immunotherapeutic efficacy. Cluster 1 was significantly correlated with poor prognosis, advanced clinical stage, higher Programmed cell death 1 ligand 1 (CD274/PD-L1) expression, a higher ESTIMATEScore and immuneScore, and distinct immune cell infiltration.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Pathway Response JAK-STAT signaling pathway hsa04630
PD-L1 expression and PD-1 checkpoint pathway in cancer hsa05235
Cell Process Cell apoptosis
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [15]
Response Summary METTL3 was essential for bladder cancer cells to resist the cytotoxicity of CD8+ T cells by regulating Programmed cell death 1 ligand 1 (CD274/PD-L1) expression. Additionally, JNK signaling contributed to tumor immune escape in a METTL3-dependent manner both in vitro and in vivo.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response PD-L1 expression and PD-1 checkpoint pathway in cancer hsa05235
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
J82 Bladder carcinoma Homo sapiens CVCL_0359
5637 Bladder carcinoma Homo sapiens CVCL_0126
In-vivo Model male C57BL/6J mice (6 weeks old) were given drinking water containing 0.05% (w/v) BBN (TCI, catalog no. B0938) for 20 weeks. After the BBN administration, mice were given normal drinking water and injected with 10% DMSO (as a control) or 20 mg/kg SP600125 (Selleck, catalog no. 129-56-6) i.p. every 3 days. After seven injections, mice were euthanized for tissue retrieval. For the bladder cancer cell-derived xenograft mouse model, male C57BL/6J mice (6 weeks old) were injected subcutaneously with 1 × 106 MB49 cells. One week after bladder cancer cell injection, 10% DMSO or 20 mg/kg SP600125 were injected i.p. every 3 days.
Protein numb homolog (NUMB)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [12]
Response Summary METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/miR-146a-5p/Protein numb homolog (NUMB)/NOTCH2 axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Melittin Investigative
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process miRNA maturation
Cell apoptosis
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
EJ (Human bladder cancer cells)
BIU-87 Human bladder cancer cells Homo sapiens CVCL_6881
In-vivo Model For melittin treatment study, 4-week-old female BALB/c nude mice were subcutaneously injected with 1 × 107 T24 or BIU87 cells.
Splicing factor, proline- and glutamine-rich (SFPQ)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [5]
Response Summary In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of MALAT1 and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. Splicing factor, proline- and glutamine-rich (SFPQ) could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Pathway Response Notch signaling pathway hsa04330
Cell Process Cell proliferation
Cell invasion
Cell apoptosis
In-vitro Model HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
In-vivo Model BALB/cnu/nu mice (4-5 weeks old) were used for the xenograft experiment. The mice were randomly divided into 2 groups (n = 6 for each group) and injected with 5 × 106 HT-1197 cells in control group or FTO plasmid group, respectively.
Superoxide dismutase [Mn], mitochondrial (SOD2)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [16]
Response Summary SNP rs5746136 affects m6A modification and regulate Superoxide dismutase [Mn], mitochondrial (SOD2) expression by guiding the binding of hnRNPC to SOD2, which played a critical tumor suppressor role in bladder cancer cells by promoting cell apoptosis and inhibiting proliferation, migration and invasion.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Heterogeneous nuclear ribonucleoproteins C1/C2 (HNRNPC) READER
Target Regulation Up regulation
Cell Process Cell apoptosis
Cell proliferation
Cell migration
Cell invasion
In-vitro Model EJ (Human bladder cancer cells)
J82 Bladder carcinoma Homo sapiens CVCL_0359
Transcription factor p65 (RELA)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary AF4/FMR2 family member 4 (AFF4), two key regulators of NF-Kappa-B pathway (IKBKB and Transcription factor p65 (RELA)) and MYC were further identified as direct targets of METTL3-mediated m6A modification.overexpression of METTL3 significantly promoted Bladder cancer cell growth and invasion.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Glucose metabolism
Vascular endothelial growth factor A (VEGFA)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [3]
Response Summary Deletion of Mettl3 leads to the suppression of TEK and Vascular endothelial growth factor A (VEGFA),ablation of Mettl3 in bladder urothelial attenuates the oncogenesis and tumor angiogenesis of bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cellular proliferation and survival
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
In-vivo Model For induction of BCa, 6-8-week-old mice were treated with drinking water containing 500 ug/ml BBN for 16 weeks and then given normal water for another 10 weeks. Tamoxifen was intraperitonelly injected to the mice with 0.08 mg/g of body weight each day for 3 days in order to inductively knock out the target gene.
Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
In total 2 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [5]
Response Summary In bladder cancer, the changes in m6A methylation level mainly appeared at 5' untranslated region (5' UTR) of Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and NOTCH1 transcripts, and at 3' UTR of CSNK2A2 and ITGA6 transcripts, responding to the overexpression of FTO. SFPQ could influence the FTO-mediated m6A RNA demethylation, eventually affecting the gene expression.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Down regulation
Pathway Response Notch signaling pathway hsa04330
Cell Process Cell proliferation
Cell invasion
Cell apoptosis
In-vitro Model HT-1197 Recurrent bladder carcinoma Homo sapiens CVCL_1291
HT-1376 Bladder carcinoma Homo sapiens CVCL_1292
In-vivo Model BALB/cnu/nu mice (4-5 weeks old) were used for the xenograft experiment. The mice were randomly divided into 2 groups (n = 6 for each group) and injected with 5 × 106 HT-1197 cells in control group or FTO plasmid group, respectively.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [17]
Response Summary FTO facilitates the tumorigenesis of bladder cancer through regulating the Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)/miR-384/MAL2 axis in m6A RNA modification manner, which ensures the potential of FTO for serving as a diagnostic or prognostic biomarker in bladder cancer.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Cell Process RNA stability
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
SCaBER Bladder squamous cell carcinoma Homo sapiens CVCL_3599
J82 Bladder carcinoma Homo sapiens CVCL_0359
253J Bladder carcinoma Homo sapiens CVCL_7935
5637 Bladder carcinoma Homo sapiens CVCL_0126
In-vivo Model Approximately 5 × 106 253J and 5637 cells infected with indicated vectors were injected subcutaneously into the flank of the mice.
microRNA 221 (MIR221)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [18]
Response Summary METTL3 has an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the microRNA 221 (MIR221) process in an m6A-dependent manner.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
In-vitro Model EJ (Human bladder cancer cells)
T24 Bladder carcinoma Homo sapiens CVCL_0554
In-vivo Model About 1× 107 cells were injected subcutaneously into the axilla of the female athymic BALB/C nude mice (4-6 weeks old, 18-22 g, five mice per group).
microRNA 222 (MIR222)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [18]
Response Summary METTL3 has an oncogenic role in bladder cancer through interacting with the microprocessor protein DGCR8 and positively modulating the microRNA 222 (MIR222) process in an m6A-dependent manner.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
In-vitro Model EJ (Human bladder cancer cells)
T24 Bladder carcinoma Homo sapiens CVCL_0554
In-vivo Model About 1× 107 cells were injected subcutaneously into the axilla of the female athymic BALB/C nude mice (4-6 weeks old, 18-22 g, five mice per group).
microRNA 576 (MIR576)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [8]
Response Summary FTO promoted bladder cancer cell proliferation, migration and invasion via the FTO/microRNA 576 (MIR576)/CDK6 pathways in an m6A-dependent manner.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Cell invasion
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
T24 Bladder carcinoma Homo sapiens CVCL_0554
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model Approximately 1 × 107 stably transfected T24 cells were subcutaneously injected into BALB/c nude mice. The length (L) and width (W) of the tumours were measured weekly using callipers, while their volume was calculated using the equation: V = (L × W2)/2. After 4 weeks of injections, the mice were euthanised, and the tumour tissues were removed and weighed.
hsa-miR-146a-5p
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [12]
Response Summary METTL3 acts as a fate determinant that controls the sensitivity of bladder cancer cells to melittin treatment. Moreover, METTL3/hsa-miR-146a-5p/NUMB/NOTCH2 axis plays an oncogenic role in bladder cancer pathogenesis and could be a potential therapeutic target for recurrent bladder cancer treatment.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Melittin Investigative
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process miRNA maturation
Cell apoptosis
In-vitro Model T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
EJ (Human bladder cancer cells)
BIU-87 Human bladder cancer cells Homo sapiens CVCL_6881
In-vivo Model For melittin treatment study, 4-week-old female BALB/c nude mice were subcutaneously injected with 1 × 107 T24 or BIU87 cells.
hsa-miR-5581-3p
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [19]
Response Summary FTO proved as an N6-methyladenosine (m6A) demethylase in decreasing m6A modification was confirmed to regulate the migration and proliferation in Bca, overexpressing hsa-miR-5581-3p partially rescued the effects of the overexpressing SMAD3 and FTO in BCa cells.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Cell Process Cell migration
cell proliferation
In-vitro Model UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
T24 Bladder carcinoma Homo sapiens CVCL_0554
SV-HUC-1 Normal Homo sapiens CVCL_3798
HEK293T Normal Homo sapiens CVCL_0063
In-vivo Model Four-week-old male BALB/c nude mice were used for animal experiments. UM-UC3 cells (2×106 cells per mouse) stably overexpressing miR-5581-3p and NC were injected into the mice to establish the subcutaneous implantation model. Tumor size was measured by a caliper every week, and tumor volume was calculated by the formula: V = (width2×length×0.52). As for the tumor metastasis model, UM-UC3 cells (1×106 cells per mouse) were injected into each mouse via the tail vein. The subcutaneous implantation model used 8 nude mice, whereas the tumor metastasis model used 10 nude mice. Assessment of tumor size and observation of metastasis tumors were done via intraperitoneal inoculation with 15mg/mL, XenoLight D-luciferin Potassium Salt (100 uL; PerkinElmer) with the IVIS Spectrum animal imaging Platform (PerkinElmer) in every mouse. Eventually, mice were sacrificed for tumors and metastases.
hsa_circ_0008399
In total 3 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [20]
Response Summary Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Cisplatin Approved
Target Regulator Wilms tumor 1-associating protein (WTAP) WRITER
Target Regulation Up regulation
Pathway Response Protein export hsa03060
Cell Process Eukaryotic translation
Cell apoptosis
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
RT-4 Bladder carcinoma Homo sapiens CVCL_0036
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model Chose 4-week-old female BALB/c nude mice for tumor xenograft experiments, which randomly were divided into four groups (n = 5 per group). Bladder cancer cells (3 × 106) were subcutaneously injected into the right axilla of the nude mice.
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [20]
Response Summary Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Cisplatin Approved
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Pathway Response Protein export hsa03060
Cell Process Eukaryotic translation
Cell apoptosis
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
RT-4 Bladder carcinoma Homo sapiens CVCL_0036
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model Chose 4-week-old female BALB/c nude mice for tumor xenograft experiments, which randomly were divided into four groups (n = 5 per group). Bladder cancer cells (3 × 106) were subcutaneously injected into the right axilla of the nude mice.
Experiment 3 Reporting the m6A-centered Disease Response by This Target Gene [20]
Response Summary Circ0008399 bound WTAP to promote formation of the WTAP/METTL3/METTL14 m6A methyltransferase complex, reduce cisplatin sensitivity in bladder cancer, implicating the potential therapeutic value of targeting this axis.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Responsed Drug Cisplatin Approved
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Up regulation
Pathway Response Protein export hsa03060
Cell Process Eukaryotic translation
Cell apoptosis
In-vitro Model 5637 Bladder carcinoma Homo sapiens CVCL_0126
RT-4 Bladder carcinoma Homo sapiens CVCL_0036
UM-UC-3 Bladder carcinoma Homo sapiens CVCL_1783
In-vivo Model Chose 4-week-old female BALB/c nude mice for tumor xenograft experiments, which randomly were divided into four groups (n = 5 per group). Bladder cancer cells (3 × 106) were subcutaneously injected into the right axilla of the nude mice.
Circ_PTPRA
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [21]
Response Summary IGF2BP1 was predominantly binded with Circ_PTPRA in the cytoplasm in BC cells.
Responsed Disease Bladder cancer [ICD-11: 2C94]
Target Regulator Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) READER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Cell invasion
In-vitro Model T24T Bladder carcinoma Homo sapiens CVCL_M892
EJ (Human bladder cancer cells)
In-vivo Model For melittin treatment study, 4-week-old female BALB/c nude mice were subcutaneously injected with 1 × 107 T24 or BIU87 cells.
References
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Ref 2 The m(6)A Methylation-Regulated AFF4 Promotes Self-Renewal of Bladder Cancer Stem Cells. Stem Cells Int. 2020 Jul 2;2020:8849218. doi: 10.1155/2020/8849218. eCollection 2020.
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Ref 4 ALKBH5 Inhibited Cell Proliferation and Sensitized Bladder Cancer Cells to Cisplatin by m6A-CK2Alpha-Mediated Glycolysis. Mol Ther Nucleic Acids. 2020 Oct 22;23:27-41. doi: 10.1016/j.omtn.2020.10.031. eCollection 2021 Mar 5.
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Ref 6 Dynamic m(6)A mRNA methylation reveals the role of METTL3-m(6)A-CDCP1 signaling axis in chemical carcinogenesis. Oncogene. 2019 Jun;38(24):4755-4772. doi: 10.1038/s41388-019-0755-0. Epub 2019 Feb 22.
Ref 7 Programmable N6-methyladenosine modification of CDCP1 mRNA by RCas9-methyltransferase like 3 conjugates promotes bladder cancer development. Mol Cancer. 2020 Dec 3;19(1):169. doi: 10.1186/s12943-020-01289-0.
Ref 8 FTO promotes tumour proliferation in bladder cancer via the FTO/miR-576/CDK6 axis in an m6A-dependent manner. Cell Death Discov. 2021 Nov 1;7(1):329. doi: 10.1038/s41420-021-00724-5.
Ref 9 METTL3/YTHDF2 m(6) A axis promotes tumorigenesis by degrading SETD7 and KLF4 mRNAs in bladder cancer. J Cell Mol Med. 2020 Apr;24(7):4092-4104. doi: 10.1111/jcmm.15063. Epub 2020 Mar 3.
Ref 10 N(6)-methyladenosine modification of ITGA6 mRNA promotes the development and progression of bladder cancer. EBioMedicine. 2019 Sep;47:195-207. doi: 10.1016/j.ebiom.2019.07.068. Epub 2019 Aug 10.
Ref 11 Mettl14 inhibits bladder TIC self-renewal and bladder tumorigenesis through N(6)-methyladenosine of Notch1. Mol Cancer. 2019 Nov 25;18(1):168. doi: 10.1186/s12943-019-1084-1.
Ref 12 Therapeutic targeting m6A-guided miR-146a-5p signaling contributes to the melittin-induced selective suppression of bladder cancer. Cancer Lett. 2022 May 28;534:215615. doi: 10.1016/j.canlet.2022.215615. Epub 2022 Mar 9.
Ref 13 Dysregulation of USP18/FTO/PYCR1 signaling network promotes bladder cancer development and progression. Aging (Albany NY). 2021 Jan 10;13(3):3909-3925. doi: 10.18632/aging.202359. Epub 2021 Jan 10.
Ref 14 m6A-Related lncRNA to Develop Prognostic Signature and Predict the Immune Landscape in Bladder Cancer. J Oncol. 2021 Jul 24;2021:7488188. doi: 10.1155/2021/7488188. eCollection 2021.
Ref 15 JNK Signaling Promotes Bladder Cancer Immune Escape by Regulating METTL3-Mediated m6A Modification of PD-L1 mRNA. Cancer Res. 2022 May 3;82(9):1789-1802. doi: 10.1158/0008-5472.CAN-21-1323.
Ref 16 Genetic variants in N6-methyladenosine are associated with bladder cancer risk in the Chinese population. Arch Toxicol. 2021 Jan;95(1):299-309. doi: 10.1007/s00204-020-02911-2. Epub 2020 Sep 22.
Ref 17 FTO modifies the m6A level of MALAT and promotes bladder cancer progression. Clin Transl Med. 2021 Feb;11(2):e310. doi: 10.1002/ctm2.310.
Ref 18 METTL3 promote tumor proliferation of bladder cancer by accelerating pri-miR221/222 maturation in m6A-dependent manner. Mol Cancer. 2019 Jun 22;18(1):110. doi: 10.1186/s12943-019-1036-9.
Ref 19 SMAD3 and FTO are involved in miR-5581-3p-mediated inhibition of cell migration and proliferation in bladder cancer. Cell Death Discov. 2022 Apr 13;8(1):199. doi: 10.1038/s41420-022-01010-8.
Ref 20 Circ0008399 Interaction with WTAP Promotes Assembly and Activity of the m(6)A Methyltransferase Complex and Promotes Cisplatin Resistance in Bladder Cancer. Cancer Res. 2021 Dec 15;81(24):6142-6156. doi: 10.1158/0008-5472.CAN-21-1518. Epub 2021 Oct 26.
Ref 21 CircPTPRA blocks the recognition of RNA N(6)-methyladenosine through interacting with IGF2BP1 to suppress bladder cancer progression. Mol Cancer. 2021 Apr 14;20(1):68. doi: 10.1186/s12943-021-01359-x.