Dataset Information

HOXC10 promotes migration and invasion via the WNT-EMT signaling pathway in oral squamous cell carcinoma.

ABSTRACT: As a master regulator of embryonic morphogenesis, homeodomain-containing gene 10 (HOXC10) has been found to promote progression of human cancers and indicate poor survival outcome. Therefore, we concentrate on elucidating the role of HOXC10 in progression of oral squamous cell carcinoma (OSCC). In our study, the expression of HOXC10 was significantly increased in human OSCC samples and was significantly correlated with TNM stage and lymph node metastasis. Upregulation of HOXC10 indicated a poor overall survival of OSCC patients according to the Kaplan-Meier survival curves. Furthermore, HOXC10-knockdown dramatically suppressed migration, invasion, and expression of N-Cadherin, Vimentin and Snail, as well as increased E-cadherin level both in vivo and in vitro. Bioinformatics and cellular study further confirmed that HOXC10 may promote invasion and migration of OSCC cells by regulating the WNT/epithelial-mesenchymal transition (EMT) signaling pathway. These findings suggest that HOXC10 plays a pivotal role in the metastasis of OSCC and highlight its usefulness as a potential prognostic marker or therapeutic target in human OSCC.

SUBMITTER: Dai BW

PROVIDER: S-EPMC6746115 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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HOXC10 promotes migration and invasion via the WNT-EMT signaling pathway in oral squamous cell carcinoma.

Dai Bo-Wen BW Yang Zhi-Min ZM Deng Ping P Chen Yan-Rong YR He Zhi-Jing ZJ Yang Xi X Zhang Sheng S Wu Han-Jiang HJ Ren Zhen-Hu ZH

Journal of Cancer 20190725 19

As a master regulator of embryonic morphogenesis, homeodomain-containing gene 10 (HOXC10) has been found to promote progression of human cancers and indicate poor survival outcome. Therefore, we concentrate on elucidating the role of HOXC10 in progression of oral squamous cell carcinoma (OSCC). In our study, the expression of HOXC10 was significantly increased in human OSCC samples and was significantly correlated with TNM stage and lymph node metastasis. Upregulation of HOXC10 indicated a poor ...[more]

PMID: 31528218

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Project description:BackgroundHistone deacetylases (HDACs) have been demonstrated to be aberrantly activated in tumorigenesis and cancer development. Thus, HDAC inhibitors (HDACIs) are considered to be promising anti-cancer therapeutics. However, recent studies have shown that HDACIs promote the migration of many cancer cells. Therefore, there is a need to elucidate the underlying mechanisms of HDACIs on cancer cell migration to establish a combination therapy that overcomes HDACI-induced cell migration.MethodsKYSE-150 and EC9706 cells were treated differently. Effects of drugs and siRNA treatment on tumor cell migration and cell signaling pathways were investigated by transwell migration assy. Gene expression for SNAI2 was tested by RT-qPCR. Western blot analysis was employed to detect the level of E-cadherin, β-catenin, vimentin,Slug，ERK1/2, H3, PAI-1 and BRD4. The effect of drugs on cell morphology was evaluated through phase-contrast microscopic images.ResultsTSA promotes epithelial-mesenchymal transition (EMT) in ESCC cells by downregulating the epithelial marker E-cadherin and upregulating mesenchymal markers β-catenin, vimentin, Slug, and PAI-1. Knockdown of Slug by siRNA or inhibition of PAI-1 clearly suppressed TSA-induced ESCC cell migration and resulted in the reversal of TSA-triggered E-cadherin, β-catenin, and vimentin expression. However, no crosstalk between Slug and PAI-1 was observed in TSA-treated ESCC cells. Blocking ERK1/2 activation also inhibited TSA-induced ESCC cell migration, EMT, and upregulation of Slug and PAI-1 levels in ESCC cells. Interestingly, inhibition of BRD4 suppressed TSA-induced ESCC cell migration and attenuated TSA-induced ERK1/2 activation and upregulation of Slug and PAI-1 levels.ConclusionsOur data indicate the existence of at least two separable ERK1/2-dependent signaling pathways in TSA-mediated ESCC cell migration: an ERK1/2-Slug branch and an ERK1/2-PAI-1 branch. Both branches of TSA-induced ESCC cell migration appear to favor the EMT process, while BRD4 is responsible for two separable ERK1/2-dependent signaling pathways in TSA-mediated ESCC cell migration.

Dataset Information

HOXC10 promotes migration and invasion via the WNT-EMT signaling pathway in oral squamous cell carcinoma.

Publications

HOXC10 promotes migration and invasion via the WNT-EMT signaling pathway in oral squamous cell carcinoma.

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