Quercetin Mediated miR-21/PTEN Signal Axis Inhibits the Expression of ABCC2 in Breast Cancer Cells and Improves Drug Absorption

This study investigated the effects of Que (quercetin) on regulating breast cancer cell prolifera tion and apoptosis by targeting the miR-21/PTEN signaling pathway, as well as its role in inhibiting ABCC2 expres sion to improve drug uptake. MCF-7 breast cancer cells were divided into four main groups: miR-21 transfection group, Que treatment group, miR-21 combined with Que treatment group, and sh-PTEN transfected group. Cell pro liferation activity was assessed using the CCK-8 assay. Western blot was performed to detect the expression levels of PTEN, AKT, p-AKT, ABCC2, E-cadherin, and vimentin. mRNA expression levels of ABCC2, PTEN, E-cadherin,and vimentin were measured by qRT-PCR. Immunofluorescence was used to examine the expression of E-cadherin and vimentin. Cell apoptosis and rhodamine 123 uptake were analyzed by flow cytometry. The results showed that: (1) compared with the NC group, the miR-21 group exhibited significantly enhanced MCF-7 cell viability (P<0.01), decreased expression levels of PTEN and E-cadherin, and significantly increased levels of p-AKT, vimentin, and ABCC2 (P<0.01), along with enhanced cell migration; (2) compared with the control group, Que inhibited miR 21 expression, reversed the miR-21-mediated downregulation of PTEN and E-cadherin and upregulation of ABCC2 and vimentin, promoted apoptosis, and suppressed cell migration; furthermore, Que attenuated the inhibitory effect of miR-21 on rhodamine 123 uptake and enhanced the cytotoxicity of doxorubicin against MCF-7 cells; the regula tory effect of Que on ABCC2 expression was associated with the activation of PTEN expression. This study reveals that Que mediates the miR-21/PTEN signaling pathway to promote apoptosis, attenuate cell migration and drug re sistance, and improve drug uptake in breast cancer MCF-7 cells.

CSTR: 32200.14.cjcb.2026.03.0005