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Effect of protein kinase C alpha, caspase-3, and survivin on apoptosis of oral cancer cells induced by staurosporine

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Acta Pharmacologica Sinica 2005年第11期26卷 1365-1372页

作者： Yu-xia ZHANG~(2,4), Shi-bin YU~(3,4), Jing-ping OU-YANG~(2,5), Dong XIA~2, Min WANG~2, Jin-rong LI~3 ~2 Department of Pathology and Pathophysiology, School of Medicine ~3 The First Department of Oral and Maxillofacial Surgery, School of Stomatology, Wuhan University Wuhan 430071, China Department of Pathology and Pathophysiology School of Medicine Wuhan University Wuhan China The First Department of Oral and Maxillofacial Surgery School of Stomatology Wuhan University Wuhan China

Aim: To elucidate inhibition of protein kinase C α （PKC α） activity by staurosporine on apoptosis of oral cancer cell line tongue squamous cell carcinoma （TSCCa） cells and to clarify the role of survivin and caspase-3 in mediating apoptosis. Methods: TSCCa cell viability was measured by MTT assay after 100 nmol/L staurosporine treatment. Apoptotic cells were identified by using phase contrast microscopy, acridine orange/ethidium bromide staining, and flow cytometry. Level of PKC α and its subcellular location were investigated using Western blot analysis. Expression of survivin and caspase-3 were evaluated using immunocytochemistry. Results: Staurosporine significantly inhibited the cell viability of TSCCa cells in a dose- and time-dependent manner. Marked cell accumulation in G2/M phase was observed after 100 nmol/L staurosporine exposure for 6 h and 12 h. In addition, the percentage of apoptosis increased in a time-dependent manner, from 2.9% in control cultures to approximately 27.4% at 100 nmol/L staurosporine treatment for 24 h. Staurosporine displayed difference in inhibitory efficacy between cytosolic and membrance-derived PKC α. The content of PKCα in membrane versus cyto-sol decreased quickly, from 0.45 in ethanol-treated control cultures to 0.18 after staurosporine exposure for 24 h （Psurvivin and an activation of caspase-3 were observed in TSCCa cells. Conclusion: Staurosporine inhibited cell viability and promoted apoptosis in TSCCa cells. Inhibition of PKCα activity might be a potential mechanism for staurosporine to induce apoptosis in this cell line. The cleavage of survivin and activation of caspase-3 signaling pathway might contribute to PKC α inhibition-induced apoptosis.

关键词： protein kinase C alpha caspase-3 survivin protein apoptosis staurosporine carcinoma, squamous cell mouth

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Protective effect of ischemic preconditioning on hepatic ischemia-reperfusion injury by advancing the expressive phase of survivin in rats

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Hepatobiliary & Pancreatic Diseases International 2008年第6期7卷 615-620页

作者： Li, Jian-Yi Gu, Xi Yin, Hong-Zhuan Zhou, Yong Zhang, Wen-Hai Qin, Yi-Min China Med Univ Shengjing Hosp Dept Gen Surg Shenyang 110004 Peoples R China Shenyang First Peoples Hosp Dept Gen Surg Shenyang 110044 Peoples R China

BACKGROUND: survivin is a new and important gene in the regulation of apoptosis. It is very important to explore the effect of the expression of survivin protein caused by ischemia-reperfusion (IR) injury. The effect of IR injury caused by ischemic preconditioning (IP) on the liver in rats and the relation between the protective effect of IP and the expression of survivin are unclear. METHODS: One hundred and fifty male Wistar rats (weighing 190-210 g, aged 6-7 weeks) were divided into three groups at random: ischemic preconditioning (IP), ischemia-reperfusion (IR) and sham-operation (SO). Sample specimens were collected from each group at 6, 12, 24, 48, and 72 hours after reperfusion. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured by an automatic biochemical analyzer. Malondialdehyde (MDA) in liver tissue was measured. Pathological changes in the liver and immunohistochemical staining for survivin were determined with an optical microscope. RESULTS: The ALT levels in the IP and IR groups after reperfusion at each time were higher than those in the SO group (Psurvivin-positive cells was larger in the IP and IR groups than in the SO group (Psurvivin-positive cells in the IP group increased compared with that in t

关键词： ischemia-reperfusion injury ischemic preconditioning survivin protein

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