Overexpression of integrin-linked kinase (ILK) promotes migration and invasion of colorectal cancer cells by inducing epithelial–mesenchymal transition via NF-κB signaling

Yan, Zhaopeng; Yin, Han; Wang, Rui; Wu, Di; Sun, Wei; Liu, Baolin; Qi, Shijie

doi:10.1016/j.acthis.2013.11.001

Cited by 37 publications

(32 citation statements)

References 31 publications

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“…The involvement of ILK was also demonstrated in the induction of cyclin D1 and DNA synthesis in 3T3 cells by SMOC-2, 15 and in SW480 CRC cells transfection with ILK resulted in the induction of EMT-like properties (enhanced migration, decrease in E-cadherin and increase in vimentin, Snail and Slug) via the NF-κB pathway. 31 Stem cells residing at the bottom of the intestinal and colonic crypts are responsible for the rapid self-renewal of these tissues by cell division, upward movement and progressive differentiation. 32 By studying the role of SMOC-2 that is both a colonic stem cell marker and a contributor to L1-mediated CRC progression, we expect to learn more about the functional significance of stem cell signature genes (such as SMOC-2 and others) in intestinal and colonic homeostasis and disease.…”

Section: Discussionmentioning

confidence: 99%

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

et al. 2015

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Overactivation of Wnt-β-catenin signaling, including β-catenin-TCF target gene expression, is a hallmark of colorectal cancer (CRC) development. We identified the immunoglobulin family of cell-adhesion receptors member L1 as a β-catenin-TCF target gene preferentially expressed at the invasive edge of human CRC tissue. L1 can confer enhanced motility and liver metastasis when expressed in CRC cells. This ability of L1-mediated metastasis is exerted by a mechanism involving ezrin and the activation of NF-κB target genes. In this study, we identified the secreted modular calcium-binding matricellular protein-2 (SMOC-2) as a gene activated by L1-ezrin-NF-κB signaling. SMOC-2 is also known as an intestinal stem cell signature gene in mice expressing Lgr5 in cells at the bottom of intestinal crypts. The induction of SMOC-2 expression in L1-expressing CRC cells was necessary for the increase in cell motility, proliferation under stress and liver metastasis conferred by L1. SMOC-2 expression induced a more mesenchymal like phenotype in CRC cells, a decrease in E-cadherin and an increase in Snail by signaling that involves integrin-linked kinase (ILK). SMOC-2 was localized at the bottom of normal human colonic crypts and at increased levels in CRC tissue with preferential expression in invasive areas of the tumor. We found an increase in Lgr5 levels in CRC cells overexpressing L1, p65 or SMOC-2, suggesting that L1-mediated CRC progression involves the acquisition of a stem cell-like phenotype, and that SMOC-2 elevation is necessary for L1-mediated induction of more aggressive/invasive CRC properties.

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Section: Discussionmentioning

confidence: 99%

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

et al. 2015

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“…ILK mediates downregulation of E-cadherin, which leads to the EMT. 45 Delcommenne et al 46 reported that after cells were transfected with activated P13K, ILK activity was significantly increased compared with the control group; however, when cells were transfected with inactivated P13K, ILK-mediated activation of its downstream factor was significantly reduced. Recent research indicates that P13K is involved in the ILKinduced EMT process; thus, the addition of LY294002 can inhibit the process.…”

mentioning

confidence: 99%

A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition

Yang

Lü

2015

Cell Adhesion & Migration

511

370

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“…The results of multivariate analysis indicated that factors independently associated with CAP measurement failure were female gender, BMI, and metabolic syndrome. However, the same type of analysis showed that factors significantly associated with elevated CAP were BMI (25)(26)(27)(28)(29)(30) kg/m 2 , BMI >30 kg/m 2 , metabolic syndrome, alcohol >14 drink/week and liver stiffness > 6 kPa. They concluded that CAP could provide an immediate assessment of steatosis simultaneously with liver stiffness measurement.…”

Section: Assessment Of Liver Fibrosismentioning

confidence: 99%

“…The central and determinant role of ILK in EMT and metastasis has been demonstrated in the case of colorectal cancer, CRC [30]. ILK and EMT signaling pathways could open ways for novel therapeutic opportunities to treat cancers including CRC.…”

Section: Preventing and Treatment Of Liver Fibrosismentioning

confidence: 99%

Liver Fibrosis: Causes and Methods of Assessment, A Review

Toosi

2015

Romanian Journal of Internal Medicine

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Hepatic fibrogenesis is the final result of injury to the liver. Fibrosis could lead to hepatic dysfunction, important in the pathogenesis of other chronic problems. Therefore, understanding the mechanism, accurate diagnosis and staging of it in early stages accelerates the treatment and reduces the prevalence of chirrosis. Treatment strategies of liver problems and detction methods depend on the amount and progression of liver fibrosis and the rate of cirrhosis development. Traditionally the invasive method, liver biopsy, is reference standard to follow progression and stage of fibrosis. However, during the past decade, progressive development of novel non-invasive methodologies has challenged the invasive method. Non-invasive methods have been initially introduced for chronic hepatitis C with increasing use in other chronic liver diseases. The need for liver biopsy has nowadays decreased significantly as a result of these methodologies. Most of the new non-invasive methods depend on either 'biological' or 'physical' approaches.In this review, starting from the mechanism of fibrogenesis, the current knowledge about diagnosis, treatment strategies and different methods for its evaluation is discussed. This is followed by a conclusion on what is expected to be known in this field during the future research.

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Overexpression of integrin-linked kinase (ILK) promotes migration and invasion of colorectal cancer cells by inducing epithelial–mesenchymal transition via NF-κB signaling

Cited by 37 publications

References 31 publications

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

Induction of the intestinal stem cell signature gene SMOC-2 is required for L1-mediated colon cancer progression

A new role for the PI3K/Akt signaling pathway in the epithelial-mesenchymal transition

Liver Fibrosis: Causes and Methods of Assessment, A Review

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