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Simvastatin and Atorvastatin inhibit DNA replication licensing factor MCM7 and effectively suppress RB-deficient

Juan Li1,2, Jie Liu1,2, Zheyong Liang1,2

  • 1Center for Translational Medicine, The First Affiliated Hospital of Xian Jiaotong University, Xi'an 710061, Shaanxi, China.

Cell Death & Disease
|March 17, 2017
PubMed

Insights

Statins like Simvastatin and Atorvastatin effectively target retinoblastoma (RB)-deficient tumors by reducing MCM7 levels, inducing cancer cell death and inhibiting tumor growth.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Loss or dysfunction of the retinoblastoma (RB) tumor suppressor is common in cancers, promoting stemness and therapy resistance.
  • Effective strategies to eliminate RB-deficient tumor cells are currently unclear.

Purpose of the Study:

  • To identify novel therapeutic strategies for RB-deficient tumors.
  • To investigate the effects of MCM7 reduction on RB-deficient cancer cells.

Main Methods:

  • Drug screening to identify compounds affecting RB-deficient cells.
  • Assessing the impact of statins (Simvastatin, Atorvastatin) on MCM7 and RB expression.
  • Evaluating chromosome stability and tumor growth in xenograft mouse models.

Main Results:

  • Reducing MCM7 induced apoptosis in RB-deficient tumor cells.
  • Statins inhibited both MCM7 and RB expression.
  • Statins caused more chromosome damage in RB-deficient cells and suppressed tumor growth in vivo.

Conclusions:

  • Statins represent a novel therapeutic approach against RB-deficient tumors.
  • The anti-tumor effect of statins is linked to MCM7 suppression.

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