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Objective: To investigate the mechanism of arsenic trioxide on apoptosis and autophagy in triple negative breast cancer (TNBC) stem cell MDA-MB-231 cell line. Methods: The stem cells cultured in the second generation were taken for 5 and divided into four groups: control group, arsenic trioxide acting group, Rapa combined with arsenic trioxide group and 3-MA combined with arsenic trioxide group. The apoptosis rate, autophagy and protein expression were observed. Results: For 48 h, the total apoptosis was 40%. When 3MA inhibited the autophagic activity, the apoptosis induced by arsenic trioxide decreased by about 50%, and Rapa promoted the arsenic trioxide induced apoptosis increased by about 50%. Compared with the control group, the intracellular fluorescence intensity was higher in arsenic trioxide, Rapa combined with arsenic trioxide, and 3-MA combined with arsenic trioxide. Bax, Beclin-1 and P62 protein expression were higher in 3-MA and arsenic trioxide group and Rapa group, and Bcl-2 protein expression was lower than the group and Rapa with arsenic trioxide group (P<0.05). Conclusion: Arsenic trioxide induced autophagy and cell apoptosis coexist in MDA-MB-231 stem cells and may be regulated by common genes. Arsenic trioxide induced autophagy can promote cell apoptosis [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of microrna-221/222 (miR-221/222) on DOX resistance of breast cancer MDA-MB-231/doxorubicin (DOX) cells. Methods: miR-221/222 inhibitor (miR-221/222 inhibitor) was transfected into MDA-MB-231/DOX cells by liposome method, the blank control group and the negative control group were set up meanwhile. The transfection efficiency and expression level of miR-221/222 in MDA-MB-231 cell line and cell line MDA-MB-231/DOX cell line was detected by real time fluorescent quantitative PCR (qRT-PCR); the change of drug sensitivity of MDA-MB-231/DOX cells to dox after 48 hours of transfection was detected by CCK-8 tests; the apoptosis rate of MDA-MB-231/DOX cells was detected by flow cytometry (FCM); the upregulation of pro-apoptotic protein p53 up regulates apoptosis (PUMA), bcl-2 protein modifying factor (BMF) and cyclin kinase inhibitor p27 (p27kip1) in MDA-MB-231/DOX cells were detected by Western blotting (WB).Results: The expression level of miR-221/222 in MDA-MB-231/DOX cells was higher than that in MDA-MB-231 cells (P<0.05), the expression level of miR-221/222 in miR-221/222 inhibitor transfected by MDA-MB-231/DOX cells was lower than that in the blank control group and the negative control group (P<0.05) after 96 hours of treatment; compared with the blank control group, the expression level of miR-221/222 inhibitor transfected by MDA-MB-231/DOX cells was lower than that in the blank control group (P<0.05). The apoptotic rate of the cells increased significantly and the expression of apoptosis promoting protein puma, BMF and p27kip1 in the cells increased (P<0.05); the 50% inhibitory concentration (IC50) of drug resistance cells in the inhibitor group was significantly lower than that in the blank control group and the negative control group (P<0.05). Conclusion: miR-221/222 can increase the resistance of MDA-MB-231/DOX cells to DOX, [ABSTRACT FROM AUTHOR]