General Information of the m6A Target Gene (ID: M6ATAR00500)
Target Name Cyclin-dependent kinase inhibitor 2A (CDKN2A)
Synonyms
Cyclin-dependent kinase 4 inhibitor A; CDK4I; Multiple tumor suppressor 1; MTS-1; p16-INK4a; p16-INK4; p16INK4A
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Gene Name CDKN2A
Chromosomal Location 9p21.3
Family CDKN2 cyclin-dependent kinase inhibitor family
Function
Acts as a negative regulator of the proliferation of normal cells by interacting strongly with CDK4 and CDK6. This inhibits their ability to interact with cyclins D and to phosphorylate the retinoblastoma protein.
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Gene ID 1029
Uniprot ID
CDN2A_HUMAN
HGNC ID
HGNC:1787
Ensembl Gene ID
ENSG00000147889
KEGG ID
hsa:1029
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
CDKN2A 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]
Representative RIP-seq result supporting the interaction between CDKN2A and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 7.42E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation.
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
Cell Process Cell proliferation
Cell migration
Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) [READER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation.
Target Regulation Up regulation
Responsed Disease Mature T-cell lymphoma ICD-11: 2A90
Cell Process Cell proliferation
Cell migration
YTH domain-containing family protein 2 (YTHDF2) [READER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [2]
Response Summary CircMET enhances mRNA decay of Cyclin-dependent kinase inhibitor 2A (CDKN2A) by direct interaction and recruitment of YTHDF2. CircMET promotes the development of NONO-TFE3 tRCC, and the regulation to both CDKN2A and SMAD3 of circMET was revealed.
Target Regulation Down regulation
Responsed Disease Renal cell carcinoma ICD-11: 2C90
Cell Process RNA stability
In-vitro Model UOK120 Papillary renal cell carcinoma Homo sapiens CVCL_B099
UOK109 Renal cell carcinoma Homo sapiens CVCL_B087
HK-2 [Human kidney] Normal Homo sapiens CVCL_0302
HEK293T Normal Homo sapiens CVCL_0063
ACHN Papillary renal cell carcinoma Homo sapiens CVCL_1067
786-O Renal cell carcinoma Homo sapiens CVCL_1051
In-vivo Model The mice were subcutaneously inoculated with 786-O cells stably transfected with lentiviruses carrying sh-NC/sh-circMET, respectively (5 × 106, 200 uL).
Mature T-cell lymphoma [ICD-11: 2A90]
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation.
Responsed Disease Mature T-cell lymphoma [ICD-11: 2A90]
Target Regulator Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) READER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary The decline in METTL3 levels was responsible for CTCL cell proliferation and migration,Cyclin-dependent kinase inhibitor 2A (CDKN2A) was a key regulator during this process in vitro and in vivo, and insufficient methylation modification blocked the interaction between CDKN2A and m6A reader IGF2BP2, resulting in mRNA degradation.
Responsed Disease Mature T-cell lymphoma [ICD-11: 2A90]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
Renal cell carcinoma [ICD-11: 2C90]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [2]
Response Summary CircMET enhances mRNA decay of Cyclin-dependent kinase inhibitor 2A (CDKN2A) by direct interaction and recruitment of YTHDF2. CircMET promotes the development of NONO-TFE3 tRCC, and the regulation to both CDKN2A and SMAD3 of circMET was revealed.
Responsed Disease Renal cell carcinoma [ICD-11: 2C90]
Target Regulator YTH domain-containing family protein 2 (YTHDF2) READER
Target Regulation Down regulation
Cell Process RNA stability
In-vitro Model UOK120 Papillary renal cell carcinoma Homo sapiens CVCL_B099
UOK109 Renal cell carcinoma Homo sapiens CVCL_B087
HK-2 [Human kidney] Normal Homo sapiens CVCL_0302
HEK293T Normal Homo sapiens CVCL_0063
ACHN Papillary renal cell carcinoma Homo sapiens CVCL_1067
786-O Renal cell carcinoma Homo sapiens CVCL_1051
In-vivo Model The mice were subcutaneously inoculated with 786-O cells stably transfected with lentiviruses carrying sh-NC/sh-circMET, respectively (5 × 106, 200 uL).
References
Ref 1 The "m6A writer" METTL3 and the "m6A reader" IGF2BP2 regulate cutaneous T-cell lymphomas progression via CDKN2A. Hematol Oncol. 2022 Apr 21. doi: 10.1002/hon.3005. Online ahead of print.
Ref 2 CircMET promotes tumor proliferation by enhancing CDKN2A mRNA decay and upregulating SMAD3. Mol Cancer. 2022 Jan 18;21(1):23. doi: 10.1186/s12943-022-01497-w.