General Information of the m6A Target Gene (ID: M6ATAR00408)
Target Name Transcription factor PU.1 (SPI1)
Synonyms
31 kDa-transforming protein
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Gene Name SPI1
Chromosomal Location 11p11.2
Family ETS family
Function
Binds to the PU-box, a purine-rich DNA sequence (5'-GAGGAA-3') that can act as a lymphoid-specific enhancer. This protein is a transcriptional activator that may be specifically involved in the differentiation or activation of macrophages or B-cells. Also binds RNA and may modulate pre-mRNA splicing (By similarity).
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Gene ID 6688
Uniprot ID
SPI1_HUMAN
HGNC ID
HGNC:11241
Ensembl Gene ID
ENSG00000066336
KEGG ID
hsa:6688
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
SPI1 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).
Browse Regulator
Browse Disease
Fat mass and obesity-associated protein (FTO) [ERASER]
Representative RNA-seq result indicating the expression of this target gene regulated by FTO
Cell Line TPC_1 cell line Homo sapiens
Treatment: FTO overexpression TPC_1 cells
Control: TPC_1 cells
GSE199206
Regulation
logFC: -7.40E+00
p-value: 4.06E-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 [1]
Response Summary FTO inhibited growth, migration and invasion of GBM cells in vitro and in vivo.decreased FTO expression could induce the downregulation of MTMR3 expression by modulating the processing of pri-miR-10a in an m6A/HNRNPA2B1-dependent manner in GBM cells. Furthermore, the transcriptional activity of FTO was inhibited by the transcription factor Transcription factor PU.1 (SPI1).
Target Regulation Down regulation
Responsed Disease Glioblastoma ICD-11: 2A00.00
In-vitro Model U-87MG ATCC Glioblastoma Homo sapiens CVCL_0022
U251 (Fibroblasts or fibroblast like cells)
U-118MG Astrocytoma Homo sapiens CVCL_0633
LN-229 Glioblastoma Homo sapiens CVCL_0393
A-172 Glioblastoma Homo sapiens CVCL_0131
In-vivo Model BALB/c male nude mice were 4 weeks old. GBM cells with stable overexpression or knockdown of FTO and ovNC or shNC were transduced with lentivirus expressing luciferase. The cells were intracranially injected at a density of 5 × 105/10 uL into every mouse to form an orthotopic xenograft model. Coordinates of injection were 1 mm anterior and 2.5 mm right to the bregma, at a depth of 3.5 mm (the right frontal lobes of the mouse). Every 6 days, bioluminescence imaging (IVIS Lumina Series III; PerkinElmer, Waltham, MA) was used to image the mouse. At 8 days, we randomly chose 5 mice from each group to euthanize them, and their brain tissues were fixed with paraformaldehyde for further study. Another 5 mice were used for survival time analysis. For DB2313 (563801; MedKoo) anti-tumor research, male nude mice were subcutaneously injected with 5 × 106 U87MG cells suspended in 0.1 mL PBS. After 7 days, mice were intraperitoneally injected with DB2313 at density of 10 mg/kg/day dissolved in PBS solvent containing 10% DMSO for 7 days. The other group treated with vehicle only was set as the control group.
Brain cancer [ICD-11: 2A00]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary FTO inhibited growth, migration and invasion of GBM cells in vitro and in vivo.decreased FTO expression could induce the downregulation of MTMR3 expression by modulating the processing of pri-miR-10a in an m6A/HNRNPA2B1-dependent manner in GBM cells. Furthermore, the transcriptional activity of FTO was inhibited by the transcription factor Transcription factor PU.1 (SPI1).
Responsed Disease Glioblastoma [ICD-11: 2A00.00]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Down regulation
In-vitro Model U-87MG ATCC Glioblastoma Homo sapiens CVCL_0022
U251 (Fibroblasts or fibroblast like cells)
U-118MG Astrocytoma Homo sapiens CVCL_0633
LN-229 Glioblastoma Homo sapiens CVCL_0393
A-172 Glioblastoma Homo sapiens CVCL_0131
In-vivo Model BALB/c male nude mice were 4 weeks old. GBM cells with stable overexpression or knockdown of FTO and ovNC or shNC were transduced with lentivirus expressing luciferase. The cells were intracranially injected at a density of 5 × 105/10 uL into every mouse to form an orthotopic xenograft model. Coordinates of injection were 1 mm anterior and 2.5 mm right to the bregma, at a depth of 3.5 mm (the right frontal lobes of the mouse). Every 6 days, bioluminescence imaging (IVIS Lumina Series III; PerkinElmer, Waltham, MA) was used to image the mouse. At 8 days, we randomly chose 5 mice from each group to euthanize them, and their brain tissues were fixed with paraformaldehyde for further study. Another 5 mice were used for survival time analysis. For DB2313 (563801; MedKoo) anti-tumor research, male nude mice were subcutaneously injected with 5 × 106 U87MG cells suspended in 0.1 mL PBS. After 7 days, mice were intraperitoneally injected with DB2313 at density of 10 mg/kg/day dissolved in PBS solvent containing 10% DMSO for 7 days. The other group treated with vehicle only was set as the control group.
References
Ref 1 SPI1-induced?downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner. Mol Ther Nucleic Acids. 2022 Jan 1;27:699-717. doi: 10.1016/j.omtn.2021.12.035. eCollection 2022 Mar 8.