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Updated: Aug 27, 2025

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TM9SF4 is an F-actin disassembly factor that promotes tumor progression and metastasis

Zhaoyue Meng1,2, Zhichao Li1,3, Mingxu Xie1

  • 1School of Biomedical Sciences and Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China.

Nature Communications
|September 29, 2022
PubMed

Insights

The protein TM9SF4 regulates cancer cell movement and spread by controlling actin dynamics. Its knockdown inhibits tumor growth and metastasis in ovarian cancer models.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Biochemistry

Background:

  • Actin dynamics are essential for cancer cell functions like migration and metastasis.
  • The precise regulatory mechanisms governing actin dynamics remain incompletely understood.

Purpose of the Study:

  • To investigate the role of TM9SF4 in regulating actin dynamics and controlling cancer cell motility and metastasis.

Main Methods:

  • Investigated TM9SF4 function in ovarian cancer cell lines (A2780, SKOV3, HGSOCs).
  • Utilized knockdown experiments to assess effects on cell migration, invasion, tumor growth, and metastasis in vivo.
  • Analyzed F-actin binding and oxidation at Cys374 induced by the TM9SF4 N-terminal fragment (NTF).

Main Results:

  • The TM9SF4 N-terminal fragment (NTF) directly binds F-actin, inducing oxidation at Cys374.
  • This oxidation enhances cofilin-mediated F-actin disassembly.
  • TM9SF4 knockdown significantly reduced migration and invasion in ovarian cancer cells.
  • In vivo, TM9SF4 knockdown completely inhibited tumor growth and metastasis in mice.

Conclusions:

  • TM9SF4 plays a critical role in regulating actin dynamics, thereby controlling ovarian cancer cell motility and metastasis.
  • The findings provide mechanistic insights into TM9SF4's function in cancer progression.

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