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Updated: May 20, 2026

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The molecular mechanism of the anticancer effect of atorvastatin: DNA microarray and bioinformatic analyses

Yan Gao1, Xue-Chun Lu, Hong-Ying Yang

  • 1First Geriatric Cardiology Division, Chinese PLA General Hospital, Beijing 100853, PR China.

International Journal of Molecular Medicine
|July 7, 2012
PubMed

Insights

Atorvastatin exhibits anticancer effects by inhibiting cell cycle progression and acting as a histone deacetylase (HDAC) inhibitor. This study reveals its potential as an anticancer drug by altering gene expression in endothelial cells.

Area of Science:

  • Molecular Biology
  • Bioinformatics
  • Pharmacology

Background:

  • Atorvastatin, a statin, is primarily known for its cholesterol-lowering effects.
  • Emerging evidence suggests potential anticancer properties of statins.
  • Understanding the molecular mechanisms underlying these effects is crucial for therapeutic development.

Purpose of the Study:

  • To elucidate the molecular mechanisms and biological pathways responsible for atorvastatin's anticancer effects.
  • To investigate the impact of atorvastatin on endothelial cell gene expression.
  • To identify potential therapeutic targets and applications of atorvastatin in cancer treatment.

Main Methods:

  • Cell-based microarray analysis of human umbilical vein endothelial cells (EA.hy926) treated with atorvastatin.
  • Bioinformatic analyses including Connectivity Map (cMap), Gene Set Enrichment Analysis (GSEA), DAVID pathway analysis, and Gene Ontology (GO) analysis.
  • Validation of differentially expressed genes using real-time polymerase chain reaction (RT-PCR).

Main Results:

  • Atorvastatin treatment (10 µM, 24 h) significantly altered gene expression, upregulating 295 genes and downregulating 354 genes.
  • Kruppel-like factors (KLFs) were upregulated, while cell cycle-related genes (e.g., CCNA2, CCNE2, CCNB1, CCNB2) were downregulated.
  • Gene expression profiles of atorvastatin-treated cells closely resembled those of histone deacetylase (HDAC) inhibitor-treated cells.

Conclusions:

  • Atorvastatin functions as a histone deacetylase (HDAC) inhibitor.
  • It acts as a G1/S and G2/M cell cycle inhibitor, disrupting cell proliferation.
  • These findings support the potential of atorvastatin as an anticancer therapeutic agent.

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