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

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Abstract

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.

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Funding

This study was funded by the foundation of the Key Laboratory of Active Components of Xinjiang Natural Medicine and Drug Release Technology [Grant No: XJDX1713].

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Authors and Affiliations

  1. College of Public Health, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China

    Guzhalinuer Maitisha

  2. College of Pharmacy, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China

    Guzhalinuer Maitisha, Zechong An & Xinxia Li

  3. Key Laboratory of Components of Xinjiang Natural Medicine and Drug Release Technology, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China

    Guzhalinuer Maitisha & Xinxia Li

  4. Central Laboratory, Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830011, Xinjiang, China

    Mutalifu Aimaiti

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  1. Guzhalinuer Maitisha
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  2. Mutalifu Aimaiti
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  3. Zechong An
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  4. Xinxia Li
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Contributions

GM contributed to the design of the study, wrote the manuscript, and analyzed the data. MA revised the manuscript and contributed to the design of the study. ZA contributed to analyzing the data. XL made substantial contributions to the conception and design of the present study and revised the manuscript. All authors read and approved the final manuscript.

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Correspondence to Xinxia Li.

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11033_2021_6722_MOESM1_ESM.tif

Supplementary file1 Fig. S1. Chromatography of allicin. The concentration of allicin stock solution was determined by HPLC, allicin was separated following the elution program of 60% methanol and 40%, 1% formic acid (TIF 692 kb)

11033_2021_6722_MOESM2_ESM.tif

Supplementary file2 Fig. S2. The dose-dependent effects of allicin on morphology of breast cancer cells (24h, ×100) (TIF 11565 kb)

Supplementary file3 (DOCX 13 kb)

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Maitisha, G., Aimaiti, M., An, Z. et al. Allicin induces cell cycle arrest and apoptosis of breast cancer cells in vitro via modulating the p53 pathway. Mol Biol Rep 48, 7261–7272 (2021). https://doi.org/10.1007/s11033-021-06722-1

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  • DOI: https://doi.org/10.1007/s11033-021-06722-1

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