MAC30 Promotes Proliferation And Inhibits Apoptosis Of Human Breast Cancer Cells Of Via PI3K/AKT

Objective: Breast cancer seriously harms women's physical and mental health,and the disease ranks number one for common female tumors.In recent years,surgery,radiotherapy and chemotherapy have been widely used to improve the 5-year survival rate of breast cancer patients.However,finding new therapeutic targets remains urgent.Meningioma-associated protein(MAC30),also known as transmembrane protein 97 gene is located on chromosome 17q11.2,and its cDNA encodes a protein consisting of 176 amino acids including five topological domains and four transmembrane domains.MAC30 is widely expressed in normal tissues,and the expression of MAC30 in cancers varies with cancer type suggesting that MAC30 plays different roles in the development of human cancers.However,the biological role of MAC30 in breast cancer is still unclear.In this study,we will knock down the MAC30 gene in breast cancer cells by lentivirus to understand its effects on the biological effects of breast cancer cell proliferation and apoptosis.Methods: 1.RT-qPCR and Western Blot were used to detect the mRNA and protein expression of MAC30 in 43 groups of breast cancer and corresponding normal adjacent tissues.2.Detection of 4 breast cancer cell lines by RT-qPCR and Western Blot mRNA and protein expression of a normal mammary epithelial cell line MAC30;3.Lenti-shRNA mediated by lentivirus to silence the expression of MAC30 in breast cancer cells MCF7 and MDA-MB-231,and detected by Western Blot Protein expression;4.CCK8 method was used to detect the proliferation of breast cancer cells MCF7 and MDA-MB-231 cells after knockdown of MAC30 expression;5.Annexin V-FITC/PI double staining method was used to detect the knockdown of MAC30 expression after mammary gland Apoptosis of cancer cells MCF7 and MDA-MB-231 cells;6.Western Blot was used to detect the effects of MAC30 on the expression of key proteins AKT,P-AKT,Cyclin D1,Bcl-2 and BAX in breast cancer cell line MCF7 and MDA-MB-231 in the PI3K/AKT regulatory pathway.Results: 1.The level of MAC30 mRNA and protein in breast cancer tissues was significantly up-regulated compared with normal adjacent tissues(p<0.05).2.Both MAC30 was expressed in breast cancer cell line and normal breast epithelial cell line MCF10 A,and in breast cancer cell lines.The expression level of MAC30 mRNA was higher than that of normal mammary epithelial cell line MCF10A(p<0.05).3.After the expression of MAC30 was down-regulated,the proliferation rate of breast cancer cells MCF7 and MDA-MB-231 decreased and the apoptosis rate increased(p<0.05).4.By Western Blot We found that the expression of P-AKT,Cyclin D1 and Bcl-2 was significantly decreased after MAC30 knockdown,while the expression of BAX was increased(p<0.05).Conclusion: The experimental results of this study showed that after knocking down the expression of MAC30,the proliferation rate of breast cancer cells decreased and the apoptosis rate increased,suggesting that MAC30 can promote the proliferation of human breast cancer cells and inhibit its apoptosis,and MAC30 may be through PI3K/ The AKT signaling pathway regulates the development of breast cancer.Therefore,MAC30 may be a potential therapeutic target for the treatment of breast cancer.