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integrin-linked kinase overexpression promotes epithelial-mesenchymal transition via nuclear factor-κB signaling in colorectal cancer cells

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World Journal of Gastroenterology 2016年第15期22卷 3969-3977页

作者： Hong Shen Jun-Li Ma Yan Zhang Gan-Lu Deng Yan-Ling Qu Xiao-Ling Wu Jing-Xuan He Sai Zhang Shan Zeng Department of Oncology Xiangya Hospital Central South University Institute of Medical Sciences Xiangya Hospital Central South University

AIM: To investigate the effect of integrin-linked kinase (ILK) on proliferation, metastasis, and invasion of the colorectal cancer cell line ***: In this study, the colorectal cancer cell line SW480 was stably transfected with ILK plasmids, and small interfering RNA (siRNA) was used to knockdown expression of nuclear factor (NF)-κB/p65. Methylthiazole tetrazolium (MTT) assay was performed to measure proliferation, and the wound healing migration assay and matrigel invasion assay were used to test the metastasis and invasion ability of SW480 cells. To explore the epithelial-mesenchymal transition (EMT) process, embryonic development, and the invasion and metastasis of tumors, the protein level of E-cadherin, vimentin, snail, and slug was detected by western blot. Immunofluorescence was also used to detect E-cadherin expression. Western blot was used to determine the level of phosphorylated-inhibitor of kappa B (IκB)a, inhibitor of gamma B (IγB)a, and nuclear factor kappa B (NF-κB) expressions and to explore the ILK signaling ***: Western blot results revealed that ILK expression significantly increased when ILK was overexpressed in SW480 cells (P < 0.05). Proliferation, metastasis, and invasion ability were improved in the vector-ILK group compared to the vector group (P < 0.05). Immunofluorescence results revealed that E-cadherin fluorescence intensity decreased after ILK was overexpressed (P < 0.05). Western blot results revealed that the protein expression of E-cadherin was reduced, while vimentin, snail, and slug were upregulated when ILK was overexpressed in SW480 cells (P < 0.05). In order to determine the role of the NF-κB signaling pathway in ILK overexpression promoted EMT occurrence, we overexpressed ILK in SW480 cells and found that levels of NF-κB/p65 and cytoplasmic phosphorylated-IκBa were increased and that cytoplasmic IкBa levels were

关键词： Colorectal cancer integrin-linked kinase Epithelial-mesenchymal transition Nuclear factor-κ B Overexpression

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integrin-linked kinase in gastric cancer cell attachment,invasion and tumor growth

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World Journal of Gastroenterology 2011年第30期17卷 3487-3496页

作者： Gang Zhao Li-Li Guo Jing-Yong Xu Hua Yang Mei-Xiong Huang Gang Xiao Department of General Surgery Beijing Hospital Peking University 100730 Beijing China Department of Ophthalmology People＇s Hospital Peking University 100044 Beijing China

AIM： To investigate the effects of integrin-linked kinase （ILK） on gastric cancer cells both in vitro and in vivo. METHODS： ILK small interfering RNA （siRNA） was transfected into human gastric cancer BGC-823 cells and ILK expression was monitored by real-time quan- titative polymerase chain reaction, Western blotting analysis and immunocytochemistry. Cell attachment, proliferation, invasion, microfilament dynamics and the secretion of vascular endothelial growth factor （VEGF） were also measured. Gastric cancer cells treated with ILK siRNA were subcutaneously transplanted into nude mice and tumor growth was assessed. RESULTS： Both ILK mRNA and protein levels were significantly down-regulated by ILK siRNA in human gastric cancer cells. This significantly inhibited cell attachment, proliferation and invasion. The knockdown of ILK also disturbed F-actin assembly and reduced VEGF secretion in conditioned medium by 40% （P 〈 0.05）. Four weeks after injection of ILK siRNA-transfected gastric cancer cells into nude mice, tumor volume and weight were significantly reduced compared with that of tumors induced by cells treated with non-silencing siRNA or by untreated cells （P 〈 0.05）. CONCLUSION： Targeting ILK with siRNA suppresses the growth of gastric cancer cells both in v/tro and /n vivo. ILK plays an important role in gastric cancer progression.

关键词： Gastric cancer integrin-linked kinase Smallinterfering RNA Cell attachment Cell proliferation Cellinvasion Cell microfilament dynamics Vascular endo-thelial growth factor Nude mice

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Inhibition of integrin-linked kinase by angiotensin II receptor antagonist, irbesartan attenuates podocyte injury in diabetic rats

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Chinese Medical Journal 2012年第5期125卷 888-893页

作者： DAI Hou-yong ZHENG Min TANG Ri-ning MA Kun-ling NI Jie LIU Bi-cheng Department of Nephrology Zhongda Hospital SoutheastUniversity School of Medicine Nanjing Jiangsu 210009 China Department of Nephrology Affiliated Hospital of NantongUniversity Nantong Jiangsu 226001 China

Background integrin-linked kinase （ILK） dysregulation is involved in the progression of diabetic nephropathy （DN）. The aim of this study was to investigate the effects of angiotensin II receptor blocker （ARB）, i... 详细信息

关键词： integrin-linked kinase diabetic nephropathy angiotension H receptor blocker podocyte injury

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Influence of irbesartan on expression of ILK and its relationship with epithelial-mesenchymal transition in mice with unilateral ureteral obstruction

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Acta Pharmacologica Sinica 2007年第11期28卷 1810-1818页

作者： Bi-cheng LIU~1,Hui-ling XIA,Ji-ning WU,Xiao-liang ZHANG,Dian-ge LIU,Yu-xiang GONGInstitute of Nephrology,Zhong Da Hospital,Southeast University.Nanjing 210009,China Institute of Nephrology Zhong Da Hospital Southeast University Nanjing China

Aim:Irbesartan,a new antagonist of the type Ⅰ angiotensin Ⅱ receptor,has beenproven to be renal protective in both diabetic and non-diabetic nephropathy,butits exact mechanism is still *** we investigated the influence ofirbesartan on the expression of the integrin-linked kinase (ILK) and its relation-ship with epithelial-mesenchymal transition (EMT) in mice with unilateral ureteralobstruction (UUO).Methods:The mice were randomly divided into 3 groups:sham operation (C,n=20),UUO (n=40),and UUO with irbesartan treatment(UUO+irbesartan,n=40).Irbesartan was given at a dose of 50 mg/kg body weightper day by *** experimental animals in the control group received thesame volume of vehicle (0.9% saline solution).The animals were sacrificed at d 1,3,7,and 14,respectively,after the ***:The expression of the ILK atmRNA and protein levels were significantly increased in the UUO group 1 d afterthe surgery,which was significantly decreased by treatment with irbesartan (P<0.01,respectively).The expression of α-smooth muscle actin (α-SMA) was sig-nificantly increased,while E-cadherin was decreased in mice with UUO at d 3 afterthe *** with irbesartan significantly abrogated such effects (P<0.01).The immunohistochemistry analysis indicated that the protein expressionof the ILK was positively correlated with α-SMA,but negatively with ***:These results suggested that irbesartan attenuated renaltubulointerstitial fibrosis in UUO mice,which may be related to the inhibition ofILK expression,subsequently preventing the tubular EMT.

关键词： irbesartan integrin-linked kinase epithelialmesenchymal transition tubulointerstitial fibrosis

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Epithelial to mesenchymal transition in the progression of tubulointerstitial fibrosis

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Chinese Medical Journal 2007年第21期120卷 1925-1930页

作者： LI Min-xia LIU Bi-cheng Institute of Nephrology Zhong Da Hospital Southeast University Nanjing 210009 China

Objective To review the mechanisms of epithelial to mesenchymal transition （EMT） and its role in the progression of tubulointerstitial fibrosis. Data sources The data used in this review were obtained mainly from the studies of EMT reported from 2000-2006. Study selection Relevant articles on studies of EMT in tubulointerstitial fibrosis were selected. Data were mainly extracted from the 45 articles listed in the reference section of this review. Results The process of EMT has gained wide recognition as candidate mechanism in progression of chronic fibrotic disorders. New markers were identified and facilitate the observation of EMT. EMT is regulated by many factors through activation of kinase-dependent signaling cascades. Recent findings suggest that EMT is a reversible process, which can be controlled by factors for their epithelial inducing activities. Conclusion Remarkable progresses of EMT research have been made recently. Preventing or reversing EMT is a promising strategy against renal fibrosis.

关键词： epithelial to mesenchymal transition connective tissue growth factor transforming growth factor integrin-linked kinase tubulointerstitial fibrosis

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Correlation of the nuclear accumulation of CTNNB1 and colonic tumorigenesis

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Chinese Medical Journal 2006年第13期119卷 1113-1117页

作者： QIU Zhe-fu Maruyama Keiji HAN De-min Nakamura Satoshi Second Department of Surgery Hamamatsu University School of Medicine 1-20-1 Handayama Hamamatsu 431-3192 Japan Beijing Otolaryngology-Head and Neck Surgery Research Centre Affiliated Beijing Tongren Hospital of Capital University of Medical Sciences Beijing 100005 China

CTNNB1 （or beta-catenin） is regarded as a central effecter in molecules of the wingless/Wnt signalling pathway, It is cadherin mediated cell to forms a complex with a key component of the cell adhesion system and the protein product of adenomatous polyposis coil （APC）, glycogen synthase kinase 3β （GSK3β） and conductin. One mutation of APC is also responsible for activation of wingless/Wnt signalling pathway and accumulation of free beta-catenin in the cell. Beta-catenin upregulates oncogenes, such as cyclin D1 and c-myc. Beta-catenin expression in cytoplasm and nuclei was reported to increase in many cases of intestinal tumorigenesis. In addition, the hyperexpression of integrin linked kinase （ILK） in colonic polyposis has been demonstrated.

关键词： beta catenin colonic polyps integrin-linked kinase piroxicam mice

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