Allicin induces cell cycle arrest and apoptosis of breast cancer cells in vitro via modulating the p53 pathway

Mol Biol Rep. 2021 Nov;48(11):7261-7272. doi: 10.1007/s11033-021-06722-1. Epub 2021 Oct 9.


Background: The tumor suppressor protein p53 is a most promising target for the development of anticancer drugs. Allicin (diallylthiosulfinate) is one of the most active components of garlic (Alliium sativum L.) and possesses a variety of health-promoting properties with pharmacological applications. However, whether allicin plays an anti-cancer role against breast cancer cells through the induction of p53-mediated apoptosis remains unknown.

Methods and results: In this study, we investigate the anti-breast cancer effect of allicin in vitro by using MCF-7 and MD-MBA-231 cells. We found that allicin reduces cell viability, induces apoptosis and cell cycle arrest in both cells. Allicin activated p53 and caspase 3 expressions in both cells but produced different effects on the expression of p53-related biomarkers. In MDA-MB-231 cells, allicin up-regulated the mRNA and protein expression of A1BG and THBS1 while down-regulated the expression of TPM4. Conversely, the mRNA and protein expression of A1BG, THBS1 and TPM4 were all reduced in MCF-7 cells. Hence, allicin induces cell cycle arrest and apoptosis in breast cancer cells through p53 activation but it effects on the expression of p53-related biomarkers were dependent upon the specific type of breast cancer involved.

Conclusions: These findings suggest that allicin induces apoptosis and regulates biomarker expression in breast cancer cell lines through modulating the p53 signaling pathway. Furthermore, our results promote the utility of allicin as compound for further studies as an anticancer drug targeting p53.

Keywords: Allicin; Apoptosis; Biomarker; Breast cancer; p53 signaling.

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology
  • Antineoplastic Agents, Phytogenic / therapeutic use
  • Apoptosis*
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / physiopathology
  • Caspase 3 / genetics
  • Cell Cycle Checkpoints*
  • Cell Line, Tumor
  • Disulfides / pharmacology*
  • Disulfides / therapeutic use
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MCF-7 Cells
  • Signal Transduction*
  • Sulfinic Acids / pharmacology*
  • Sulfinic Acids / therapeutic use
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Antineoplastic Agents, Phytogenic
  • Disulfides
  • Sulfinic Acids
  • Tumor Suppressor Protein p53
  • allicin
  • CASP3 protein, human
  • Caspase 3