[Effects of vesicular stomatitis virus matrix protein on proliferation and apoptosis of mouse LL/2c cells]

Ju-Mei Zhao1, Tao Liu, Jian-Rong Xu

  • 1State Key Laboratory of Biotherapy, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, PR China.

Abstract

Insights

Vesicular stomatitis virus (VSV) M protein effectively inhibited mouse tumor cell proliferation and induced apoptosis. This finding supports VSV-M protein as a safer alternative for oncolytic cancer therapy.

Area of Science:

  • Oncolytic virotherapy
  • Molecular oncology
  • Cell biology

Context:

  • Vesicular stomatitis virus (VSV) shows promise for tumor therapy.
  • Clinical use of live VSV is limited by safety concerns.
  • The VSV matrix (M) protein is implicated in antitumor effects.

Purpose:

  • To investigate the impact of VSV-M protein on mouse LL/2c tumor cell proliferation and apoptosis.
  • To assess the feasibility of using VSV-M protein as a therapeutic agent.

Summary:

  • A plasmid encoding VSV-M protein was successfully constructed and transfected into LL/2c cells.
  • VSV-M protein expression was confirmed via RT-PCR and Western blot.
  • Transfected cells exhibited inhibited proliferation (41.3% reduction) and induced apoptosis, evidenced by DNA laddering and nuclear changes.

Impact:

  • VSV-M protein demonstrates significant antitumor potential by inhibiting proliferation and inducing apoptosis in LL/2c cells.
  • This research offers a potentially safer alternative to live VSV for oncolytic cancer treatment.