Abstract
Our previous study indicated that nontoxic doses of quercetin (Que) could increase the chemosensitivity of breast cancer cells to doxorubicin (Dox) although the mechanism still remains elusive. Therefore, in this study, we aimed to investigate the underlying mechanisms. MCF-7 cells and MCF-7/dox cells were exposed to PTEN inhibitor bpV (HOpic), Dox, or combination of Dox and Que with or without bpV (HOpic) intervention for 24 hours. Cell proliferation, cell apoptosis, cell invasion and expression of PTEN and phospho-Akt (p-Akt) were then assessed. bpV (HOpic) had little effect on cell proliferation at concentrations less than 1 μM. Compared to treatment with Dox alone, combined treatment with Dox and Que significantly inhibited cell proliferation and invasion, increased cell apoptosis, up-regulated the expression of PTEN and down-regulated the expression of p-Akt. However, co-treatment with PTEN inhibitor bpV (HOpic) could revert the effects of Que on Dox. These data indicate that Que can increase the sensitivity of breast cancer cells to Dox through down regulation of p-Akt expression arising from increased expression of PTEN.
Keywords: Chemosensitivity, doxorubicin, p-Akt, PTEN, quercetin.
Graphical Abstract
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