Pharmacology 2018;102(1-2):58-66. doi: 10.1159/000489564.

Galangin Induces Apoptosis in MCF-7 Human Breast Cancer Cells Through Mitochondrial Pathway and Phosphatidylinositol 3-Kinase/Akt Inhibition

Dan Liu  1 Pengtao You  1 Yan Luo  2 Min Yang  3 Yanwen Liu  1

  • 1 School of Pharmacy, Hubei Key Laboratory of Resource Science and Chemistry in Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, China.
  • 2 Affiliated Renhe Hospital of China Three Gorges University, Yichang, China.
  • 3 School of Pharmacy, Hubei University of Chinese Medicine, Wuhan, China.


Aims: The study aimed to investigate the molecular mechanism of inhibition of proliferation and apoptosis induction by galangin against MCF-7 human breast cancer cells.

Methods: Cell Counting Kit-8 assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis. The expression level of apoptosis-related proteins (cleaved-caspase-9, cleaved-caspase-8, cleaved-caspase-3, Bad, cleaved-Bid, Bcl-2, Bax, p-phosphatidylinositol 3-kinase [PI3K], and p-Akt) and cell cycle-related proteins (cyclin D3, cyclin B1, cyclin-dependent kinases CDK1, CDK2, CDK4, p21, p27, p53) were evaluated by Western blotting.

Results: Galangin increased the expression of Bax and decreased the expression of Bcl-2 in a concentration-dependent manner, inhibited cell viability, and induced apoptosis. Meanwhile, the expression of cleavage of caspase-9, caspase-8, caspase-3, Bid, and Bad increased significantly while the expression of p-PI3K and p-Akt proteins decreased. In addition, the protein levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated while the expression levels of p21, p27, and p53 were upregulated significantly.

Conclusion: Galangin could suppress the viability of MCF-7 cells and induce cell apoptosis via the mitochondrial pathway and PI3K/Akt inhibition as well as cell cycle arrest.

Keywords: Apoptosis; Cyclin-dependent kinases; Cyclins; Galangin; MCF-7 human breast cancer cells; Mitochondrial; Phosphatidylinositol 3-kinase/Akt.