Yanyan Zhao1, Lufang Wang1, Yanshi Wang1, Siyu Dong1, Shaojie Yang1, Yifu Guan2, Xin Wu1. 1. Department of Gynecology, The First Affiliated Hospital of China Medical University, China Medical University, Shenyang, Liaoning, P.R. China. 2. Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, Liaoning, P.R. China.
Abstract
OBJECTIVE: To explore the inhibition of the proliferation of vulvar squamous cell carcinoma (VSCC) by astragaloside IV. METHODS: MTT examined the cell proliferation of VSCC. Flow cytometry analyzed cell cycle and apoptosis. Western blot assay detected the expression of some relevant proteins. RESULTS: AS-IV reduced the proliferation of SW962 cells in a concentration- and time-dependent manner, induced cell-cycle arresting in G0/G1 phase, as demonstrated by the up-regulation of P53 and P21 expression, and the down-regulation of cyclin D1 expression. AS-IV enhanced the expression of Bax and cleaved-caspase 3, and suppressed Bcl-2 and Bcl-xl expression, which resulted in apoptosis increased. Furthermore, the expression of Beclin-1 and LC3-B was upregulated and that of P62 was downregulated, which suggested that AS-IV could increase the incidence of autophagy in SW962 cells. After inhibiting autophagy by 3-methyladenine (3-MA), cell apoptosis decreased upon AS-IV treatment. Similarly, TGF-β1 stimulated SW962 cells, cell proliferation enhanced, and the expression of TGF-βRII and Smad4 was decreased. Furthermore, the expression of proteins that promote apoptosis and autophagy decreased. After AS-IV treatment, the expression levels of the above proteins exhibited the opposite effect. CONCLUSION: AS-IV inhibits cell proliferation and induces apoptosis and autophagy through the TGF-β/Smad signaling pathway in VSCC.
OBJECTIVE: To explore the inhibition of the proliferation of vulvar squamous cell carcinoma (VSCC) by astragaloside IV. METHODS:MTT examined the cell proliferation of VSCC. Flow cytometry analyzed cell cycle and apoptosis. Western blot assay detected the expression of some relevant proteins. RESULTS: AS-IV reduced the proliferation of SW962 cells in a concentration- and time-dependent manner, induced cell-cycle arresting in G0/G1 phase, as demonstrated by the up-regulation of P53 and P21 expression, and the down-regulation of cyclin D1 expression. AS-IV enhanced the expression of Bax and cleaved-caspase 3, and suppressed Bcl-2 and Bcl-xl expression, which resulted in apoptosis increased. Furthermore, the expression of Beclin-1 and LC3-B was upregulated and that of P62 was downregulated, which suggested that AS-IV could increase the incidence of autophagy in SW962 cells. After inhibiting autophagy by 3-methyladenine (3-MA), cell apoptosis decreased upon AS-IV treatment. Similarly, TGF-β1 stimulated SW962 cells, cell proliferation enhanced, and the expression of TGF-βRII and Smad4 was decreased. Furthermore, the expression of proteins that promote apoptosis and autophagy decreased. After AS-IV treatment, the expression levels of the above proteins exhibited the opposite effect. CONCLUSION: AS-IV inhibits cell proliferation and induces apoptosis and autophagy through the TGF-β/Smad signaling pathway in VSCC.