m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00267)
Target Name Zinc finger protein GLI1 (GLI1)
Synonyms
Glioma-associated oncogene; Oncogene GLI; GLI
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Gene Name GLI1
Chromosomal Location 12q13.3
Family GLI C2H2-type zinc-finger protein family
Function
Acts as a transcriptional activator. Binds to the DNA consensus sequence 5'-GACCACCCA-3'. Regulates the transcription of specific genes during normal development. Plays a role in craniofacial development and digital development, as well as development of the central nervous system and gastrointestinal tract. Mediates SHH signaling. Plays a role in cell proliferation and differentiation via its role in SHH signaling. [Isoform 2]: Acts as a transcriptional activator, but activates a different set of genes than isoform 1. Activates expression of CD24, unlike isoform 1. Mediates SHH signaling. Promotes cancer cell migration.
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Gene ID 2735
Uniprot ID
GLI1_HUMAN
HGNC ID
HGNC:4317
Ensembl Gene ID
ENSG00000111087
KEGG ID
hsa:2735
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
GLI1 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
Methyltransferase-like 3 (METTL3) [WRITER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line HUVEC cell line Homo sapiens
Treatment: shMETTL3 HUVEC cells
Control: shScramble HUVEC cells
 GSE157544
Regulation
logFC: 7.30E-01
p-value: 2.91E-03
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between GLI1 and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 7.23E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 silence decreased the m6A modification and expression of Zinc finger protein GLI1 (GLI1), an important component of hedgehog pathway, which led to cell apoptosis.the m6A methyltransferase METTL3 promotes the growth and motility of prostate cancer cells by regulating hedgehog pathway.
Target Regulation Up regulation
Responsed Disease Prostate cancer ICD-11: 2C82
 Disease Info 
Pathway Response Hedgehog signaling pathway hsa04340
Cell Process Cell proliferation
Cell survival
Cell colony formation
Cell invasion
In-vitro Model LNCaP C4-2 Prostate carcinoma Homo sapiens CVCL_4782
LNCaP C4-2B Prostate carcinoma Homo sapiens CVCL_4784
DU145 Prostate carcinoma Homo sapiens CVCL_0105
LNCaP Prostate carcinoma Homo sapiens CVCL_0395
PC-3 Prostate carcinoma Homo sapiens CVCL_0035
In-vivo Model Equal number of PC-3 cells was injected subcutaneously into right flank.
Prostate cancer [ICD-11: 2C82]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 silence decreased the m6A modification and expression of Zinc finger protein GLI1 (GLI1), an important component of hedgehog pathway, which led to cell apoptosis.the m6A methyltransferase METTL3 promotes the growth and motility of prostate cancer cells by regulating hedgehog pathway.
Responsed Disease Prostate cancer [ICD-11: 2C82]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Pathway Response Hedgehog signaling pathway hsa04340
Cell Process Cell proliferation
Cell survival
Cell colony formation
Cell invasion
In-vitro Model LNCaP C4-2 Prostate carcinoma Homo sapiens CVCL_4782
LNCaP C4-2B Prostate carcinoma Homo sapiens CVCL_4784
DU145 Prostate carcinoma Homo sapiens CVCL_0105
LNCaP Prostate carcinoma Homo sapiens CVCL_0395
PC-3 Prostate carcinoma Homo sapiens CVCL_0035
In-vivo Model Equal number of PC-3 cells was injected subcutaneously into right flank.
References
Ref 1 RNA m(6)A Methyltransferase METTL3 Promotes The Growth Of Prostate Cancer By Regulating Hedgehog Pathway. Onco Targets Ther. 2019 Nov 5;12:9143-9152. doi: 10.2147/OTT.S226796. eCollection 2019.