Breast cancer (BC) is the primary cause of women cancer death, which could be prevented by EGCG that has been recently shown several health properties included anti-cancer, however the mechanism underpinning still poorly understood. In this study, several biological activities of both MCF7 and MDA-MB-231 cells were evaluated in response to EGCG. Cell viability and the role of Akt and AMPK inhibitor molecules, and sodium pyruvate on this viability, apoptosis, metastasis, and interestingly regulation of glucose metabolism were assessed. EGCG promoted cytotoxicity in both BC cell lines after 24h but not less. Co-incubated cells with Akt and AMPK inhibitors alongside EGCG significantly caused more reduction in cell viability compared to the effect of EGCG alone with maximum effect referred to Akt inhibitor. While supplemented sodium pyruvate significantly restored the decreases in cell viability. Remarkably, EGCG induced apoptosis through increased caspase 3/7 activation associated with upregulated Bax gene, in addition to anti-metastatic effect through decreasing cellular migration. Importantly, lactate production was sharply reduced after 6h (no alteration of viable cells) and 24h (decreased viable cells) concomitant with significant blocked glucose uptake in response to EGCG. In conclusion, EGCG could be a potential anti-migration, the anti-cancerous therapeutic agent through targeting cancer cells glucose metabolism.
|Journal||Journal of Physics: Conference Series|
|Publication status||Published - 5 Jul 2019|
|Event||1st International Scientific Conference on Pure Science - Al-Qadisiyah, Iraq|
Duration: 23 Jan 2019 → 24 Jan 2019
Bibliographical noteOpen Access: Content from this work may be used under the terms of the Creative Commons Attribution 3.0 licence. Any further distribution of this work must maintain attribution to the author(s) and the title of the work, journal citation and DOI.
Funding: Iraqi Ministry of Higher Education and Scientific Research.
- Glucose metabolism