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- W928199558 abstract "Proc Amer Assoc Cancer Res, Volume 45, 20044979 Numerous evidences have suggested that human cancers developed through the accumulation of epigenetic and genetic alterations. Recently, it is reported that genetic and epigenetic changes of RAS effecter proteins is associated with colorectal carcinogenesis. In this study, we investigate in great detail the occurrence and spectrum of epigenetic alteration of RASSF family (RASSF1-6) in colorectal cancer. Database analysis revealed that six RASSF family genes that contain Ras-association (RA) have CpG islands in their 5’ end. Among six genes, RASSF2 was most frequently silenced by hypermethylation of 5’ CpG island in colorectal cancer (CRC) cell lines (7/10, 70%). Treatment of cancer cells with a methyltransferase inhibitor, DAC, but not with a histone decatylase inhibitor, TSA induced gene expression. To investigate alteration of RAS signaling pathway in primary CRCs, we analyzed genetic and epigenetic changes of K-ras, BRAF and RASSF1-RASSF6 in a series of primary colorectal cancers and colorectal adenomas. Hypermethylation of RASSF2 was found in 51 of 122 (42%) primary colorectal cancers and 21 of 49 (43%) adenomas, and primary colorectal cancers with CIMP+ showed significantly more frequent RASSF2 methylation than CIMP- tumors (P<0.001). Eighty-five of 122 (70%) primary colorectal cancers showed at least one alteration in RAS/BRAF/RASSF1-6, indicating that a majority of CRCs showed defects in RAS signaling pathway. Transfection of RASSF2 to CRC cell lines induced apoptosis and inhibited cell growth by colony formation assay. These results suggested that RASSF2 is one of the most frequently silenced RAS signaling molecules in CRC and RAS signaling pathway can be a good molecular target for therapy in colorectal carcinogenesis." @default.
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- W928199558 date "2004-04-01" @default.
- W928199558 modified "2023-09-27" @default.
- W928199558 title "K-ras/Ras effector alterations in colorectal cancers" @default.
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