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Astragaloside IV inhibits cell proliferation in vulvar squamous cell carcinoma through the TGF‐β/Smad signaling pathway
Author(s) -
Zhao Yanyan,
Wang Lufang,
Wang Yanshi,
Dong Siyu,
Yang Shaojie,
Guan Yifu,
Wu Xin
Publication year - 2018
Publication title -
dermatologic therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.595
H-Index - 68
eISSN - 1529-8019
pISSN - 1396-0296
DOI - 10.1111/dth.12802
Subject(s) - cell growth , apoptosis , cell cycle , smad , autophagy , cancer research , flow cytometry , cell , downregulation and upregulation , signal transduction , microbiology and biotechnology , chemistry , biology , biochemistry , gene
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.