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The potential oncogenic and MLN4924-resistant effects of CSN5 on cervical cancer cells

Huilin Zhang1, Ping He2, Qing Zhou3,4

  • 1Department of Surgical Pathology, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

Cancer Cell International
|July 12, 2021
PubMed
Abstract

Insights

CSN5 acts as an oncogene in cervical cancer, inhibiting cell proliferation and causing cell cycle arrest. Overexpression of CSN5 may predict resistance to MLN4924 (pevonedistat) treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • CSN5, a component of the Cop9 signalosome, is crucial for protein neddylation and implicated as an oncogene in various cancers.
  • The specific role of CSN5 in cervical cancer pathogenesis remained unexplored.

Purpose of the Study:

  • To investigate the expression profile and clinical significance of CSN5 in cervical cancer.
  • To elucidate the functional role of CSN5 in cervical cancer cell proliferation, cell cycle, and response to MLN4924.

Main Methods:

  • Analysis of TCGA and GEO datasets for CSN5 expression in cervical cancer.
  • CSN5 knockdown using CRISPR-Cas9 in Siha and Hela cell lines.
  • In vitro assays (CCK8, colony formation, 3D spheroid, cell cycle) and in vivo xenograft models.
  • Western blot analysis and MLN4924 treatment in CSN5-overexpressing cells.

Main Results:

  • Downregulation of CSN5 inhibited cervical cancer cell proliferation both in vitro and in vivo, with effects rescued by CSN5 re-expression.
  • CSN5 deletion induced cell cycle arrest but not apoptosis.
  • CSN5 overexpression conferred resistance to the anti-cancer effects of MLN4924 (pevonedistat).

Conclusions:

  • CSN5 functions as an oncogene in cervical cancer.
  • CSN5 may serve as a predictive biomarker for MLN4924 treatment efficacy in cervical cancer patients.
Keywords:
CSN5Cervical cancerMLN924Neddylation

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