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Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes.

ABSTRACT: Chibby1 (Cby1) was originally isolated as a binding partner for β-catenin, a dual function protein in cell-cell adhesion and in canonical Wnt signaling. The canonical Wnt/β-catenin pathway is dysregulated in various diseases including cancer, most notably of the gastrointestinal origin. To investigate the role of Cby1 in colorectal tumorigenesis, we generated stable Cby1-knockdown (K_D) SW480 colon cancer cells. Unexpectedly, we found that Cby1 K_D induces mesenchymal-to-epithelial transition (MET)-like changes in SW480 as well as in HEK293 cells. Cby1-K_D cells displayed a cuboidal epithelial morphology with tight cell-cell contacts. In Cby1-K_D cells, the plasma membrane localization of E-cadherin and β-catenin was dramatically increased with formation of cortical actin rings, while the levels of the mesenchymal marker vimentin were decreased. Consistent with these changes, in wound healing assays, Cby1-K_D cells exhibited epithelial cell-like properties as they migrated collectively as epithelial sheets. Furthermore, the anchorage-independent growth of Cby1-K_D cells was reduced as determined by soft agar assays. These findings suggest that chronic Cby1 K_D in colon cancer cells may counteract tumor progression by promoting the MET process.

SUBMITTER: Fischer V

PROVIDER: S-EPMC5351918 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes.

Fischer Victoria V Wong Michael M Li Feng-Qian FQ Takemaru Ken-Ichi KI

Cell cycle (Georgetown, Tex.) 20170120 5

Chibby1 (Cby1) was originally isolated as a binding partner for β-catenin, a dual function protein in cell-cell adhesion and in canonical Wnt signaling. The canonical Wnt/β-catenin pathway is dysregulated in various diseases including cancer, most notably of the gastrointestinal origin. To investigate the role of Cby1 in colorectal tumorigenesis, we generated stable Cby1-knockdown (K<sub>D</sub>) SW480 colon cancer cells. Unexpectedly, we found that Cby1 K<sub>D</sub> induces mesenchymal-to-epit ...[more]

PMID: 28107095

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Project description:BackgroundLung cancer is the most common and lethal malignancy worldwide. TCTP is highly expressed in various cancers including lung cancer. Epithelial-mesenchymal transition (EMT) could increase cancer cell invasion. Whether TCTP's expression is associated with EMT in lung adenocarcinoma is largely unknown.MethodsSeveral Gene Expression Omnibus datasets were used to analyze the correlation between TCTP expression and overall survival of lung adenocarcinoma patients by Kaplan-Meier survival analysis. Then, 24 surgically removed fresh lung adenocarcinoma tissue samples and paired paracancer tissue samples were used to analyze the correlation between TCTP expression and tumor stage by immunohistochemical analysis. Furthermore, stable cell lines were generated using lentiviral transduction systems to knock down or overexpress TCTP in A549 cells. Cell migration and invasion were measured by scratch and transwell assays, and EMT marker proteins such as α-SMA, ZEB1, and E-cadherin were quantitated by Western blot. The expression levels of miR-200a, miR-141, and miR-429 were determined by real-time quantitative PCR, and their target genes were predicted by an online database miRTarBase. The interaction between TCTP and these genes was analyzed by String database and visualized by Cytoscape.ResultsTCTP was highly expressed in tumor tissues compared to paracancer tissues. The expression of TCTP was associated with shorter overall survival. TCTP knockdown experiment in A549 cells suggested that TCTP knockdown could decrease the migration and invasion of lung cancer cells, and the expression level of ZEB1 and α-SMA, but increase the expression of E-cadherin and p53. Vice versa, overexpression of TCTP could increase the migration and invasion of cancer cells, and the expression level of ZEB1 and α-SMA, but decrease the expression of E-cadherin and p53. Furthermore, we found the expression of miR-200a, miR-141, and miR-429 was associated with TCTP expression.ConclusionTCTP promotes EMT in lung adenocarcinoma, and this effect may be associated with miR-200 family members like miR-200a, miR-141, and miR-429.

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Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes.

Publications

Chibby1 knockdown promotes mesenchymal-to-epithelial transition-like changes.

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