RASSF10 suppresses hepatocellular carcinoma growth by activating P53 signaling and methylation of RASSF10 is a docetaxel resistant marker

Yongshuai Jin, Baoping Cao, Meiying Zhang, Qimin Zhan, James G. Herman, Miao Yu, Mingzhou Guo

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)231-240
Number of pages10
JournalGenes and Cancer
Volume6
Issue number5-6
StatePublished - 2015
Externally publishedYes

Keywords

  • DNA methylation
  • Epigenetics
  • Hepatocellular carcinoma
  • P53 signaling
  • RASSF10

ASJC Scopus subject areas

  • Cancer Research
  • Genetics

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