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WTAP regulates autophagy in colon cancer cells by inhibiting FLNA through N6-methyladenosine

Liang Huang1, Jinfan Shao1, Xijuan Xu1

  • 1Department of General Surgery, Taizhou First People's Hospital, Taizhou, Zhejiang, China.

Cell Adhesion & Migration
|February 27, 2023
PubMed

Insights

WTAP (Wingless-type MMTV integration site family, member 1) protein is upregulated in colon cancer, promoting tumor growth and inhibiting apoptosis. WTAP-mediated m6A modification plays a crucial role in colon cancer progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Epigenetics

Background:

  • WTAP (Wingless-type MMTV integration site family, member 1) is implicated in various cancers.
  • The specific role and regulatory mechanisms of WTAP in colon cancer remain incompletely understood.

Purpose of the Study:

  • To investigate the role of WTAP in colon cancer development.
  • To elucidate the regulatory mechanism of WTAP, including its downstream targets and effects on cellular processes.
  • To explore the potential of targeting WTAP for colon cancer therapy.

Main Methods:

  • m6A dot blot hybridization
  • Methylated RNA immunoprecipitation (MeRIP)
  • Dual-luciferase reporter assays
  • RNA immunoprecipitation (RIP)
  • Western blotting
  • Rescue experiments

Main Results:

  • WTAP expression is significantly upregulated in colon cancer tissues.
  • WTAP promotes colon cancer cell proliferation and inhibits apoptosis.
  • FLNA (Filamin A) was identified as a direct downstream target of WTAP.
  • WTAP-mediated m6A modification leads to the post-transcriptional repression of FLNA.
  • WTAP and FLNA together inhibit autophagy, a process implicated in cancer progression.

Conclusions:

  • WTAP plays a critical oncogenic role in colon cancer by regulating FLNA expression and inhibiting autophagy.
  • WTAP-mediated m6A modification is a key driver of colon cancer development.
  • Targeting the WTAP/FLNA axis presents a potential therapeutic strategy for colon cancer.
Keywords:
FLNAWTAPautophagycolon cancerm6A

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