Guzhalinuer Maitisha1,2,3, Mutalifu Aimaiti4, Zechong An2, Xinxia Li5,6. 1. College of Public Health, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China. 2. College of Pharmacy, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China. 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. 4. Central Laboratory, Xinjiang Medical University, No. 393 Xinyi Road, Urumqi, 830011, Xinjiang, China. 5. College of Pharmacy, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China. lixinxia_XJMU@outlook.com. 6. Key Laboratory of Components of Xinjiang Natural Medicine and Drug Release Technology, Xinjiang Medical University, No. 567 North Shangde Road, Urumqi, 830017, Xinjiang, China. lixinxia_XJMU@outlook.com.
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.
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.
Authors: Dekuang Zhao; William M Tahaney; Abhijit Mazumdar; Michelle I Savage; Powel H Brown Journal: Cell Mol Life Sci Date: 2017-06-22 Impact factor: 9.261