E2F8 contributes to human hepatocellular carcinoma via regulating cell proliferation

Qing Deng, Qun Wang, Wei Ying Zong, Da Li Zheng, Yi Xin Wen, Ke Sheng Wang, Xiao Mei Teng, Xin Zhang, Jian Huang, Ze Guang Han

Research output: Contribution to journalArticlepeer-review

89 Scopus citations

Abstract

The E2F family member of transcription factors includes the atypical member E2F8, which has been little studied in cancer. We report that E2F8 is strongly upregulated in human hepatocellular carcinoma (HCC), where it was evidenced to contribute to oncogenesis and progression. Ectopic overexpression of E2F8 promoted cell proliferation, colony formation, and tumorigenicity, whereas E2F8 knockdown inhibited these phenotypes, as documented in Huh-7, Focus, Hep3B, and YY-8103 HCC cell lines. Mechanistic analyses indicated that E2F8 could bind to regulatory elements of cyclin D1, regulating its transcription and promoting accumulation of S-phase cells. Together, our findings suggest that E2F8 contributes to the oncogenic potential of HCC and may constitute a potential therapeutic target in this disease.

Original languageEnglish (US)
Pages (from-to)782-791
Number of pages10
JournalCancer Research
Volume70
Issue number2
DOIs
StatePublished - Jan 15 2010
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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