Potential mechanism of Astragalus polysaccharide increasing chemosensitivity of cervical cancer HeLa cells to carboplatin by modulating the PI3K/Akt signaling pathway

Abstract

The current study investigated the possible mechanisms in which astragalus polysaccharide (APS) elevates the chemosensitivity of cervical cancer (CC) HeLa cells to carboplatin (CBP) by regulating the PI3K/Akt pathway. In this study, HeLa cells were assigned to the control, CBP, APS, and APS + CBP groups, and the proliferation of HeLa cells in each group was detected using the MTT (methyl thiazolyl tetrazolium) assay. The apoptosis and cycle of HeLa cells were examined using flow cytometry, and the expression levels of PI3K (phosphatidylinositol-3-kinases), Akt (Protein Kinase B), p-PI3K (phospho-phosphatidylinositol-3-kinases), and p-Akt (phospho-Akt) proteins in the PI3K/Akt pathway were determined using Western blot. MTT results revealed that the inhibitory effect was more significant within the APS + CBP groups (p < 0.01). The flow cytometry results showed that the apoptosis rate was significantly elevated in the APS + CBP groups (p < 0.01). Compared with the control group, the most prominent arrest in the G2/M phase and the arrest within the G2/M phase in the APS + CBP groups being the most significant. Western-blot results depicted that the above proteins in the APS + CBP groups revealed more significant expression changes (p < 0.01). The above analyses demonstrated that APS could increase the chemosensitivity of CC HeLa cells to CBP by modulating the PI3K/Akt pathway. In conclusions, it is reasonable to believe that the enhancing effect of APS on the sensitivity of chemotherapeutic drugs was associated with blocking the PI3K/Akt pathway, thus, enhancing.