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RASSF10 suppresses hepatocellular carcinoma growth by activating P53 signaling
and methylation of RASSF10 is a docetaxel resistant marker
#MMPMID26124922
Jin Y
; Cao B
; Zhang M
; Zhan Q
; Herman JG
; Yu M
; Guo M
Genes Cancer
2015[May]; 6
(5-6
): 231-40
PMID26124922
show ga
Hepatocellular carcinoma (HCC) is one of the most common malignances and the
second leading cause of cancer related death worldwide. RASSF10 is located on
chromosome 11p15.2, a region that shows frequent loss of heterozygosity (LOH) in
several cancer types. Our previous study found that RASSF10 suppresses colorectal
cancer growth by activating P53 signaling. To explore the epigenetic changes and
the mechanism of RASSF10 in human HCC, 69 cases of primary HCC, twenty cases of
normal liver tissue samples and 17 HCC cell lines were involved in this study. We
found that RASSF10 was methylated in 82.6% (57/69) of human primary HCC and
methylation of RASSF10 was significantly associated with tumor size (P < 0.05)
and TNM stage (P < 0.05). The expression of RASSF10 was regulated by promoter
region methylation. Restoration of RASSF10 expression suppressed cell
proliferation, induced apoptosis and G2/M phase arrest, as well as sensitized
cells to docetaxel and activated P53 signaling in HepG2 and QGY7703 cells. In
conclusion, we demonstrated that RASSF10 is frequently methylated in human HCC
and its methylation is a potential docetaxel resistant marker. Our data also
indicate that RASSF10 suppresses human HCC growth by activating P53 signaling.
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