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Effects of re-expressed RASSF1A on gene expression in rhabdoid tumor of the kidney cells.

ABSTRACT: Several groups reported the correlation between hypermethylation of RASSF1A and aggressiveness or a poor outcome in various pediatric tumors, including Wilms tumor. In addition, it is known that the overexpression of RASSF1A promotes apoptotic cell cycle arrest and reduces the tumorigenicity. In an attempt to identify epigenetic targets related to the biological features of rhabdoid tumor of the kidney (RTK), we analyzed the methylation level of the RASSF1A gene in RTK. RASSF1A promoter region in RTK is hypermethylated and the gene and protein expression levels were low. To examine the effect of re-expression of RASSF1A in RTK cells from the viewpoint of gene expression, we performed micro array analysis. We observed neither clear apoptosis induction nor cell-cycle arrest in RASSF1A-expressed RTK cell lines. Furthermore, the geneexpression profiling induced by RASSF1A expression in RTK cell line is curious, and CDK6 expression was significantly increased while CDKN2A expression was significantly decreased after RASSF1A expression. The changes in the gene expression profile that we observed in RTK cells after RASSF1A expression may not be causative events involving the suppression of cell proliferation, but rather antagonizingevents reflecting cellular responses against RASSF1A expression in RTK cells that are deficient in SMARCB1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171508 | GEO | 2024/04/05

REPOSITORIES: GEO

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