STANDARD_NAME	TANAKA_METHYLATED_IN_ESOPHAGEAL_CARCINOMA
SYSTEMATIC_NAME	M14455
COLLECTION	C2:CGP
MSIGDB_URL	https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/TANAKA_METHYLATED_IN_ESOPHAGEAL_CARCINOMA
NAMESPACE	Human_NCBI_Gene_ID
DESCRIPTION_BRIEF	Genes with hypermethylated DNA in all four esophageal squamous cell carcinoma (ESCC) lines analyzed.
DESCRIPTION_FULL	Epigenetic alterations and the resulting inactivation of tumor suppressor genes often contribute to the development of various cancers. To identify novel candidates that may be silenced by aberrant methylation in esophageal squamous-cell carcinoma (ESCC), we analysed ESCC cell lines by a recently developed method known as bacterial artificial chromosome array-based methylated CpG island amplification (BAMCA), and selected candidates through BAMCA-assisted strategy. In the course of this program, we identified frequent CpG methylation-dependent silencing of the gene encoding cellular retinoic acid binding protein 1 (CRABP1) in our panel of ESCC cell lines. Expression of CRABP1 mRNA was restored in gene-silenced ESCC cells after treatment with 5-aza 2'-deoxycytidine. The DNA methylation status of the CRABP1 CpG island with clear promoter activity correlated inversely with expression of this gene. CpG methylation of CRABP1 was frequently observed in primary ESCC tissues as well. Restoration of CRABP1 expression in ESCC cells lacking the protein reduced cell growth by inducing arrest at G(0)-G(1), whereas knockdown of the gene in cells expressing CRABP1 promoted cell growth. Among 113 primary ESCC tumors, the absence of immunoreactive CRABP1 was significantly associated with de-differentiation of cancer cells and with distant lymph-node metastases in the patients. These results indicate that CRABP1 appears to have a tumor-suppressor function in esophageal epithelium, and its epigenetic silencing may play a pivotal role during esophageal carcinogenesis. Its expression status in biopsies or resected tumors might serve as an index for identifying ESCC patients for whom combined therapeutic modalities would be recommended.
PMID	17438526
GEOID	
AUTHORS	Tanaka K,Imoto I,Inoue J,Kozaki K,Tsuda H,Shimada Y,Aiko S,Yoshizumi Y,Iwai T,Kawano T,Inazawa J
CONTRIBUTOR	Arthur Liberzon
CONTRIBUTOR_ORG	MSigDB Team
EXACT_SOURCE	Table 1S
FILTERED_BY_SIMILARITY	
EXTERNAL_NAMES_FOR_SIMILAR_TERMS	
EXTERNAL_DETAILS_URL	
SOURCE_MEMBERS	10473,10482,105,10629,10763,10930,112399,1128,119467,120227,123920,1305,1381,1382,158471,2070,2074,2108,222171,2222,222642,222643,23111,252969,25934,26257,2626,26574,267004,3068,3167,3175,343472,3658,3778,3848,3849,3860,3881,3882,3883,3884,3885,3886,389549,390598,3975,399823,4223,442425,4781,4800,4914,5083,5099,5436,5456,54663,55128,55335,5546,55466,56606,56652,56956,57057,5729,5732,57526,57715,5791,6299,64795,64799,64843,6520,6811,6894,696,7080,7738,79590,796,79831,79842,80144,80349,81831,81875,84333,84545,8687,8688,8689,8900,9047,9184,925,9480,9585,9749,9833,9948
GENE_SYMBOLS	HMGN4,NXF1,ADARB2,TAF6L,NES,APOBEC2,EGLN3,CHRM1,CLRN3,CYP2R1,CMTM3,COL13A1,CRABP1,CRABP2,PRUNE2,EYA4,ERCC6,ETFA,PRR15,FDFT1,TSPO2,UNC5CL,SPART,NEIL2,NIPSNAP3A,NKX2-8,GATA4,AATF,,HDGF,HMX2,ONECUT1,BARHL2,IREB2,KCNMA1,KRT1,KRT2,KRT13,KRT31,KRT32,KRT33A,KRT33B,KRT34,KRT35,FEZF1,SKOR1,LHX1,FOXI2,MEOX2,FOXB2,NFIB,NFYA,NTRK1,PAX9,PCDH7,POLR2G,POU3F4,WDR74,TRIM68,NIPSNAP3B,PRCC,DNAJA4,SLC2A9,TWNK,LHX9,TBX20,PTGDR,PTGER2,PCDH19,SEMA4G,PTPRE,SALL1,RMND5A,IQCH,ISL2,SLC3A2,STX5,TARBP1,BTN1A1,NKX2-1,ZNF184,MRPL24,CALCA,KDM8,ZBTB3,FRAS1,SKIC8,NETO2,ISG20L2,PCGF5,MRPL43,KRT38,KRT37,KRT36,CCNA1,SH2D2A,BUB3,CD8A,ONECUT2,KIF20B,PHACTR2,MELK,WDR1
FOUNDER_NAMES