Vol 49 No. 4: 302-310 [PDF] [Full Text]
Response of human non-small-cell lung cancer cells to the influence of Wogonin with SGK1 dynamics
Guanglin Shi, Qian Wang, Xiaoyu Zhou, Jun Li, Hua Liu, Jun Gu, Haiying Wang, Yi Wu, Liang Ding, Songshi Ni*, and Zhiyuan Tang*
Department of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong 226001, China
These authors contributed equally to this work

Abstract  A number of significant studies in the field of cell biology have revealed another pattern of intracellular signal transduction in which cells transmit information through the dynamics of key signaling molecules. Dynamical properties of p53 have been demonstrated to be the key factor in dictating cell fate, including cell cycle arrest, permanent cell cycle arrest, and cell death. Previous studies showed a negative feedback regulation pathway between SGK1 and p53, but the dynamics of SGK1 have never been reported before. Therefore, we used different dosing strategies of Wogonin to affect SGK1 dynamics and investigate its impact on cell response. Key factors, such as APAF1, BAX, GADD45A, p21, PML, and YPEL3, which are related to cell cycle arrest, senescence, and apoptosis, were measured at different time points after incubation with Wogonin. Western blot and quantitative reverse transcriptase-polymerase chain reaction analysis were used to examine protein and mRNA expression of these genes. In addition, we also used β-galactosidase staining and flow cytometric analysis to further verify the results. It was found that Wogonin inhibited cell viability and downregulated SGK1 protein levels; 20 μM Wogonin could induce non-small-cell lung cancer A549 cells into cell cycle arrest/senescence/apoptosis after 0.5/2/4 h, respectively; and SGK1 dynamics showed significant differences under different cell responses. Together, our findings showed that SGK1 protein dynamics can be an important part of intracellular signaling, directly influencing cellular response decisions.


Keywords   SGK1, NSCLC, dynamic, cell response


Received   2016-11-15  


Funding  This work was supported by the grants from the National Natural Science Foundation of China (No. 81503143), Chinese Postdoctoral Science Foundation (No. 2015M581846), Six Talent Peaks Project in Jiangsu Province (No. 2015-WSN-062), Key Technology Research of Nantong—People's Livelihood (No. MS22015113), and the Research Innovation Program for College Graduates of Jiangsu Province (No. YKC15081).


* Correspondence address  Tel: +86-513-81161601; Fax: +86-513-85052297; E-mail: jsntnss@163.com (S.N.)/Tel: +86-513-81161602; Fax; +86-513-85052297; E-mail: tina2951@sina.com (Z.T.)

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