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Knockdown of stat3 expression using RNAi inhibits growth of laryngeal tumors in vivo

Acta Pharmacologica Sinica 2006年第3期27卷 347-352页

作者： Li-fang GAO~1 Lian-ji WEN~2 Hao YU~1 Ling ZHANG~1 Yan MENG~1 Yue-ting SHAO~1 De-qi XU~(3,4) Xue-jian ZHAO~(1,4) ~1Department of Pathophysiology.Basic School of Medicine,Jilin University,Changchun 130021.China.~2Department of ENT.Secona Hospital of Jilin University.Changchun 130012,China ~3Laboratory of Enteric and Sexually Transmitted Diseases.Center for Biologies Evaluation and Research.Food and Drug Administration,Bethesda.Maryland,USA Department of Pathophysiology Basic School of Medicine Jilin University Changchun China Departmet of ENT Second Hospital of Jilin University Changchun China Laboratory of Enteric and Sexually Transmitted Diseases Center for Biologics Evaluation and Research Food and Drug Administration Bethesda USA

Aim:To study the effect of pSilencer1.0-U6-siRNA-stat3 on the growth of humanlaryngeal tumors in nude ***:Hep2 cells were transplanted into nudemice,then at the time of tumor formation,growth rates were *** thetumor formed,pSilencer1.0-U6-siRNA-stat3 was *** volumes werecalculated,and growth curves were *** histological sectionswere taken from mice bearing transplantation tumors in both treated and controlgroups,and stat3,pTyr-stat3,Bcl-2,cvclin D1,and survivin expression weredetected by Western blotting,survivin mRNA levels were detected by Northernblotting,hematoxylin and eosin staining and terminal deoxyribonucleotidyl trans-ferase-mediated dUTP-digoxigenin nick end-labeling(TUNEL)assay to confirmthe apoptosis of ***:In nude mice,pSilencer1.0-U6-siRNA-stat3significantly suppressed the growth of tumors compared with controls(Pstat3 expression,and downregulated BcL2,cyclin *** survivinexpression within the *** significantly induced apoptosis of the ***:pSilencer1.0-U6-siRNA-stat3 was able to inhibit the growth of trans-planted human laryngeal tumors in nude mice and induce apoptosis.

关键词： RNA interference stat3 protein laryngeal neoplasms nude mice

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Activation of stat3 signaling in human stomach adenocarcinoma drug-resistant cell line and its relationship with expression of vascular endothelial growth factor

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World Journal of Gastroenterology 2005年第6期11卷 875-879页

作者： Li-FenYu YingCheng Min-MinQiao Yong-PingZhang Yun-LinWu DepartmentofGastroenterology RuijinHospitalofShanghaiSecondMedicalUniversityShanghai200025China

AIM: To investigate the difference in activation of stat3 signaling between two human stomach adenocarcinoma cell lines: 5-fluorouracil resistant cell line and its parental cell line, and to evaluate its relationship with the expression of vascular endothelial growth factor (VEGF). METHODS: Western blot and electrophoretic mobility shift assay (EMSA) were used to detect the expression of phospho-stat3 protein and constitutive activation of stat3 in two human stomach adenocarcinoma cell lines, 5-fluorouracil resistant cell line SGC7901/R and its parental cell line SGC7901, respectively. The mRNA expression of VEGF was analysed by semi-quantitative RT-PCR. The expressive intensity of VEGF protein was measured by immunocytochemistry. RESULTS: The expressions of phospho-statS protein and constitutive activation of stat3 between two human stomach adenocarcinoma cell lines were different. Compared with the parental cell line SGC7901, the stat3DNA binding activity and the expressive intensity of phospho-stat3 protein were lower in the drug-resistant cell line SGC7901/R. The expression levels of VEGF mRNA and its encoded protein were also decreased in drugresistant cell line. CONCLUSION: Over-expression of VEGF may be correlated with elevated stat3 activation in parental cell line. Lower VEGF expression may be correlated with decreased stat3 activation in resistant cell line, which may have resulted from negative feedback regulation of stat signaling.

关键词： Stomach adenocarcinoma Vascular endothelial growth factor stat3 protein Antineoplastic Drug Resistance

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