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YTHDF2 suppresses cell proliferation and growth via destabilizing the EGFR mRNA in hepatocellular carcinoma

Li Zhong1, Dan Liao1, Meifang Zhang1

  • 1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.

Cancer Letters
|November 14, 2018
PubMed

Insights

Hypoxia down-regulates YTHDF2 in liver cancer cells. YTHDF2 acts as a tumor suppressor by degrading EGFR mRNA, inhibiting cancer cell growth and proliferation.

Area of Science:

  • Molecular Biology
  • Oncology
  • Epigenetics

Background:

  • N6-methyladenosine (m6A) is a prevalent mRNA modification in eukaryotes.
  • m6A methyltransferases and demethylases are crucial in cancer development.
  • The function of m6A-binding proteins in cancer is largely unknown.

Purpose of the Study:

  • To investigate the role of YTHDF2, an m6A-binding protein, in hepatocellular carcinoma (HCC).
  • To elucidate the mechanism by which YTHDF2 influences HCC progression.

Main Methods:

  • Studied YTHDF2 expression under hypoxic conditions in HCC cells.
  • Assessed the effects of YTHDF2 overexpression on HCC cell proliferation, tumor growth, and MEK/ERK signaling.
  • Investigated the direct binding of YTHDF2 to EGFR mRNA and its impact on mRNA stability.

Main Results:

  • Hypoxia specifically down-regulated YTHDF2 in HCC cells.
  • YTHDF2 overexpression suppressed HCC cell proliferation, tumor growth, and MEK/ERK activation.
  • YTHDF2 directly bound to the m6A site in EGFR 3'-UTR, promoting EGFR mRNA degradation.

Conclusions:

  • YTHDF2 functions as a tumor suppressor in HCC.
  • YTHDF2 represses HCC cell proliferation and growth by destabilizing EGFR mRNA.
  • YTHDF2 down-regulation by hypoxia may contribute to HCC progression.
Keywords:
EGFRERKHCCYTHDF2mRNA

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