m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00497)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
IGF1R
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3 | ||
Cell Line | LX2 cell line | Homo sapiens |
Treatment: shMETTL3 LX2 cells
Control: shLuc LX2 cells
|
GSE207909 | |
Regulation |
|
logFC: 6.69E-01 p-value: 4.12E-12 |
More Results | Click to View More RNA-seq Results |
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Prostate cancer | ICD-11: 2C82 | ||
Cell Process | RNA stability | |||
In-vitro Model | PC-3 | Prostate carcinoma | Homo sapiens | CVCL_0035 |
LNCaP C4-2B | Prostate carcinoma | Homo sapiens | CVCL_4784 | |
In-vivo Model | At 1 week post-injection with PC-3 cells, mice were randomly assigned to three groups (n = 8 per group): the ASO-NC group (injection with ASO negative control targeting unknown sequence, 5 nmol in 100 uL PBS for each mouse), the ASO-L group (injection with low-dose ASO targeting PCAT6, 5 nmol in 100 uL PBS for each mouse), and the ASO-H group (injection with high-dose ASO targeting PCAT6, 10 nmol in 100 uL PBS for each mouse). | |||
RNA demethylase ALKBH5 (ALKBH5) [ERASER]
Representative RNA-seq result indicating the expression of this target gene regulated by ALKBH5 | ||
Cell Line | MOLM-13 cell line | Homo sapiens |
Treatment: shALKBH5 MOLM-13 cells
Control: shNS MOLM-13 cells
|
GSE144968 | |
Regulation |
|
logFC: -6.16E-01 p-value: 4.93E-02 |
More Results | Click to View More RNA-seq Results |
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [2] | |||
Response Summary | ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing Insulin-like growth factor 1 receptor (IGF1R) m6A-modifications | |||
Target Regulation | Up regulation | |||
Responsed Disease | Endometrial cancer | ICD-11: 2C76 | ||
In-vitro Model | T HESCs | Normal | Homo sapiens | CVCL_C464 |
RL95-2 | Endometrial adenosquamous carcinoma | Homo sapiens | CVCL_0505 | |
HEC-1-A | Endometrial adenocarcinoma | Homo sapiens | CVCL_0293 | |
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) [READER]
In total 2 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [3] | |||
Response Summary | IGF2BP2, as a m6A reader, was proved to increase the expression of Insulin-like growth factor 1 receptor (IGF1R) by identifying m6A methylation modification sites in IGF1R mRNA, thus activating RhoA-ROCK pathway. The oncogenic role of IGF2BP2 in gastric cancer carcinogenesis and confirmed its activation is partly due to the activation of IGF1R-RhoA-ROCK signaling pathway. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Gastric cancer | ICD-11: 2B72 | ||
In-vitro Model | SGC-7901 | Gastric carcinoma | Homo sapiens | CVCL_0520 |
MKN45 | Gastric adenocarcinoma | Homo sapiens | CVCL_0434 | |
MKN1 | Gastric adenosquamous carcinoma | Homo sapiens | CVCL_1415 | |
MGC-803 | Gastric mucinous adenocarcinoma | Homo sapiens | CVCL_5334 | |
GES-1 | Normal | Homo sapiens | CVCL_EQ22 | |
In-vivo Model | A total of 30 BALB/c nude mice were chosen and assigned to three groups: (1) control (injected with 0.2 mL PBS), (2) si-NC (injected with si-NC transfected SGC7901 cells) and (3) si-IGF2BP2 (injected with si-IGF2BP2 transfected SGC7901 cells (n = 5 per group). 2 × 106 SGC7901 cells were injected into the left right back of each mouse through subcutaneous injection. Tumor sizes were recorded once per week. After 28 days, the mice were euthanized, and tumor tissues were weighted. | |||
Experiment 2 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Prostate cancer | ICD-11: 2C82 | ||
Cell Process | RNA stability | |||
In-vitro Model | PC-3 | Prostate carcinoma | Homo sapiens | CVCL_0035 |
LNCaP C4-2B | Prostate carcinoma | Homo sapiens | CVCL_4784 | |
In-vivo Model | At 1 week post-injection with PC-3 cells, mice were randomly assigned to three groups (n = 8 per group): the ASO-NC group (injection with ASO negative control targeting unknown sequence, 5 nmol in 100 uL PBS for each mouse), the ASO-L group (injection with low-dose ASO targeting PCAT6, 5 nmol in 100 uL PBS for each mouse), and the ASO-H group (injection with high-dose ASO targeting PCAT6, 10 nmol in 100 uL PBS for each mouse). | |||
YTH domain-containing protein 2 (YTHDC2) [READER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [4] | |||
Response Summary | YTHDC2 promotes radiotherapy resistance of NPC cells by activating the Insulin-like growth factor 1 receptor (IGF1R)/ATK/S6 signaling axis and serves as a potential therapeutic target in radiosensitization of NPC cells. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Nasopharyngeal carcinoma | ICD-11: 2B6B | ||
In-vitro Model | HK1-IRR (HK1-IRR (HK1-ionizing radiation radioresistent cell line) was derived from HK1 after a prolonged exposure of irradiation.HK1, a generous gift from Prof. Ya Cao (Cancer Research Institute, Central South University), was established from a recurrent nasopharynx carcinoma of a Chinese 17-year-old male patient) | |||
NPC/HK1 | Nasopharyngeal carcinoma | Homo sapiens | CVCL_7084 | |
CNE2-IRR (CNE2-IRR (CNE2-ionizing radiation radioresistent cell line) was derived from CNE2 after a prolonged exposure of irradiation) | ||||
CNE-2 | Nasopharyngeal carcinoma | Homo sapiens | CVCL_6889 | |
In-vivo Model | 2 × 106 cells resuspended in 50 uL of Matrigel (Corning) were subcutaneously injected into 4-6 weeks old male nude mice. When tumor volumes reached 150-200 mm3, animals were divided into control group and radiotherapy group. In the radiotherapy group, tumors were treated with a single irradiation (4 Gy) when tumor volumes reached approximately 150-200 mm3. The tumor stopped growing in the next few days and then restarted growth. | |||
Nasopharyngeal carcinoma [ICD-11: 2B6B]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [4] | |||
Response Summary | YTHDC2 promotes radiotherapy resistance of NPC cells by activating the Insulin-like growth factor 1 receptor (IGF1R)/ATK/S6 signaling axis and serves as a potential therapeutic target in radiosensitization of NPC cells. | |||
Responsed Disease | Nasopharyngeal carcinoma [ICD-11: 2B6B] | |||
Target Regulator | YTH domain-containing protein 2 (YTHDC2) | READER | ||
Target Regulation | Up regulation | |||
In-vitro Model | HK1-IRR (HK1-IRR (HK1-ionizing radiation radioresistent cell line) was derived from HK1 after a prolonged exposure of irradiation.HK1, a generous gift from Prof. Ya Cao (Cancer Research Institute, Central South University), was established from a recurrent nasopharynx carcinoma of a Chinese 17-year-old male patient) | |||
NPC/HK1 | Nasopharyngeal carcinoma | Homo sapiens | CVCL_7084 | |
CNE2-IRR (CNE2-IRR (CNE2-ionizing radiation radioresistent cell line) was derived from CNE2 after a prolonged exposure of irradiation) | ||||
CNE-2 | Nasopharyngeal carcinoma | Homo sapiens | CVCL_6889 | |
In-vivo Model | 2 × 106 cells resuspended in 50 uL of Matrigel (Corning) were subcutaneously injected into 4-6 weeks old male nude mice. When tumor volumes reached 150-200 mm3, animals were divided into control group and radiotherapy group. In the radiotherapy group, tumors were treated with a single irradiation (4 Gy) when tumor volumes reached approximately 150-200 mm3. The tumor stopped growing in the next few days and then restarted growth. | |||
Gastric cancer [ICD-11: 2B72]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [3] | |||
Response Summary | IGF2BP2, as a m6A reader, was proved to increase the expression of Insulin-like growth factor 1 receptor (IGF1R) by identifying m6A methylation modification sites in IGF1R mRNA, thus activating RhoA-ROCK pathway. The oncogenic role of IGF2BP2 in gastric cancer carcinogenesis and confirmed its activation is partly due to the activation of IGF1R-RhoA-ROCK signaling pathway. | |||
Responsed Disease | Gastric cancer [ICD-11: 2B72] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
In-vitro Model | SGC-7901 | Gastric carcinoma | Homo sapiens | CVCL_0520 |
MKN45 | Gastric adenocarcinoma | Homo sapiens | CVCL_0434 | |
MKN1 | Gastric adenosquamous carcinoma | Homo sapiens | CVCL_1415 | |
MGC-803 | Gastric mucinous adenocarcinoma | Homo sapiens | CVCL_5334 | |
GES-1 | Normal | Homo sapiens | CVCL_EQ22 | |
In-vivo Model | A total of 30 BALB/c nude mice were chosen and assigned to three groups: (1) control (injected with 0.2 mL PBS), (2) si-NC (injected with si-NC transfected SGC7901 cells) and (3) si-IGF2BP2 (injected with si-IGF2BP2 transfected SGC7901 cells (n = 5 per group). 2 × 106 SGC7901 cells were injected into the left right back of each mouse through subcutaneous injection. Tumor sizes were recorded once per week. After 28 days, the mice were euthanized, and tumor tissues were weighted. | |||
Endometrial cancer [ICD-11: 2C76]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [2] | |||
Response Summary | ALKBH5 promoted proliferation and invasion of endometrial cancer via erasing Insulin-like growth factor 1 receptor (IGF1R) m6A-modifications | |||
Responsed Disease | Endometrial cancer [ICD-11: 2C76] | |||
Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
Target Regulation | Up regulation | |||
In-vitro Model | T HESCs | Normal | Homo sapiens | CVCL_C464 |
RL95-2 | Endometrial adenosquamous carcinoma | Homo sapiens | CVCL_0505 | |
HEC-1-A | Endometrial adenocarcinoma | Homo sapiens | CVCL_0293 | |
Prostate cancer [ICD-11: 2C82]
In total 2 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa. | |||
Responsed Disease | Prostate cancer [ICD-11: 2C82] | |||
Target Regulator | Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) | READER | ||
Target Regulation | Up regulation | |||
Cell Process | RNA stability | |||
In-vitro Model | PC-3 | Prostate carcinoma | Homo sapiens | CVCL_0035 |
LNCaP C4-2B | Prostate carcinoma | Homo sapiens | CVCL_4784 | |
In-vivo Model | At 1 week post-injection with PC-3 cells, mice were randomly assigned to three groups (n = 8 per group): the ASO-NC group (injection with ASO negative control targeting unknown sequence, 5 nmol in 100 uL PBS for each mouse), the ASO-L group (injection with low-dose ASO targeting PCAT6, 5 nmol in 100 uL PBS for each mouse), and the ASO-H group (injection with high-dose ASO targeting PCAT6, 10 nmol in 100 uL PBS for each mouse). | |||
Experiment 2 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | METTL3-mediated m6A modification contributed to PCAT6 upregulation in an IGF2BP2-dependent manner. Furthermore, PCAT6 upregulated Insulin-like growth factor 1 receptor (IGF1R) expression by enhancing IGF1R mRNA stability through the PCAT6/IGF2BP2/IGF1R RNA-protein three-dimensional complex. The m6 A-induced PCAT6/IGF2BP2/IGF1R axis promotes PCa bone metastasis and tumor growth, suggesting that PCAT6 serves as a promising prognostic marker and therapeutic target against bone-metastatic PCa. | |||
Responsed Disease | Prostate cancer [ICD-11: 2C82] | |||
Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
Target Regulation | Up regulation | |||
Cell Process | RNA stability | |||
In-vitro Model | PC-3 | Prostate carcinoma | Homo sapiens | CVCL_0035 |
LNCaP C4-2B | Prostate carcinoma | Homo sapiens | CVCL_4784 | |
In-vivo Model | At 1 week post-injection with PC-3 cells, mice were randomly assigned to three groups (n = 8 per group): the ASO-NC group (injection with ASO negative control targeting unknown sequence, 5 nmol in 100 uL PBS for each mouse), the ASO-L group (injection with low-dose ASO targeting PCAT6, 5 nmol in 100 uL PBS for each mouse), and the ASO-H group (injection with high-dose ASO targeting PCAT6, 10 nmol in 100 uL PBS for each mouse). | |||
References