AKT serine/threonine protein kinase modulates baicalintriggered autophagy in human bladder cancer T24 cells

Chingju Lin, Shih Chang Tsai, Michael T. Tseng, Shu Fen Peng, Sheng Chu Kuo, Meng Wei Lin, Yuan Man Hsu, Miau Rong Lee, Sakae Amagaya, Wen Wen Huang, Tian Shung Wu, Jai Sing Yang

研究成果: Article同行評審

48 引文 斯高帕斯(Scopus)

摘要

Baicalin is one of the major compounds in the traditional Chinese medicinal herb from Scutellaria baicalensis Georgi. We investigated the molecular mechanisms of cell autophagy induced by baicalin in human bladder cancer T24 cells. Baicalin inhibited cell survival as shown by MTT assay and increased cell death by trypan blue exclusion assay in a concentration-dependent manner. Baicalin did not induce apoptotic cell death in T24 cells by TUNEL and caspase-3 activity assay. Baicalin induced the acidic vesicular organelle cell autophagy marker, manifested by acridine orange (AO) and monodansylcadaverine (MDC) staining and cleavage of microtubule-associated protein 1 light chain 3 (LC3). The protein expression levels of the Atg 5, Atg 7, Atg 12, Beclin-1 and LC3-II were upregulated in T24 cells after baicalin treatment. Inhibition of autophagy by 3-methyl-adenine (an inhibitor of class III phosphatidylinositol-3 kinase; 3-MA) reduced the cleavage of LC3 in T24 cells after baicalin treatment. Furthermore, protein expression levels of phospho-AKT (Ser473) and enzyme activity of AKT were downregulated in T24 cells after baicalin treatment. In conclusion, baicalin triggered cell autophagy through the AKT signaling pathway in T24 cells.

原文English
頁(從 - 到)993-1000
頁數8
期刊International Journal of Oncology
42
發行號3
DOIs
出版狀態Published - 2013 三月

All Science Journal Classification (ASJC) codes

  • 腫瘤科
  • 癌症研究

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