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Overexpression of TEAD4 correlates with poor prognosis of glioma and promotes cell invasion.

ABSTRACT: This study aimed to reveal the correlation of increased TEA domain transcription factor 4 (TEAD4) expression and disease prognosis in glioma. The expression data of TEAD4 mRNA in glioma were collected from GEO database (GSE4290), and the expression of TEAD4 protein in glioma was confirmed using western blot and Immunohistochemistry. Kaplan-Meier analysis with the log-rank test was used to reveal the correlation of TEAD4 expression level and patients' survival. The effects of TEAD4 on migration and invasion were separately examined by Transwell assay and Boyden assay. Gene set enrichment analysis (GSEA) was performed to predict the possible biological function of TEAD4 in glioma. The results showed that TEAD4 mRNA and protein expression were upregulated in glioma tissues compared to normal brain tissues. Furthermore, overexpression of TEAD4 correlated with poor prognosis in glioma patients. Knockdown of TEAD4 markedly inhibited glioma cells migration and invasion in vitro. Consistent with the result that TEAD4 was associated with epithelial-mesenchymal transition (EMT) closely by GESA, knockdown of TEAD4 resulted in N-cadherin, vimentin and Slug downregulated but E-cadherin upregulated. Our study indicated that overexpression of TEAD4 may represent as a potential unfavorable marker for poor survival and prognosis in glioma. Knockdown of TEAD4 led to suppressed glioma migration and invasion.

SUBMITTER: Xu A

PROVIDER: S-EPMC6962916 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Overexpression of TEAD4 correlates with poor prognosis of glioma and promotes cell invasion.

Xu Anqi A Wang Xizhao X Zeng Yu Y Zhou Mingfeng M Yi Renhui R Wu Zhiyong Z Lin Jie J Song Ye Y

International journal of clinical and experimental pathology 20181001 10

This study aimed to reveal the correlation of increased TEA domain transcription factor 4 (TEAD4) expression and disease prognosis in glioma. The expression data of TEAD4 mRNA in glioma were collected from GEO database (GSE4290), and the expression of TEAD4 protein in glioma was confirmed using western blot and Immunohistochemistry. Kaplan-Meier analysis with the log-rank test was used to reveal the correlation of TEAD4 expression level and patients' survival. The effects of TEAD4 on migration a ...[more]

PMID: 31949557

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Project description:Objective Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor. Laminin 5γ2 chain (LAMC2) was reported to be associated with tumorigenesis. This study explored the role of LAMC2 on LSCC progression by regulating the integrinβ1/FAK/Src/AKT pathway. Methods The level of LAMC2 in 46 LSCC patients was detected by qRT-PCR and western blot. Then the relationship between LAMC2 expression and LSCC malignancy as well as prognosis was analyzed, and the effect of LAMC2 expression on LSCC patient survival was also analyzed using the Kaplan–Meier survival curves. Afterwards, the LSCC cells were transfected with LAMC2 overexpression and knockdown vectors, the effect of LAMC2 on LSCC cell viability, proliferation ability, cell cycle, cell migration, and invasion were detected by CCK-8, colony formation, flow cytometry, wound healing, and Transwell assays. The expression of EMT-related biomarkers and integrin β1/FAK/Src/AKT signaling-related proteins was detected by western blot. Moreover, the effect of LAMC2 on LSCC tumor growth was evaluated by in vivo xenograft experiments and western blot. Results LAMC2 was expressed at high level in LSCC tissues and associated with poor prognosis. LAMC2 overexpression increased TU177 cell viability, proliferation ability, promoted cell cycle, cell migration, and invasion capacity. The expression of N-cadherin, vimentin, and integrinβ1/FAK/Src/AKT related proteins was increased, while the expression of E-cadherin protein was decreased. When the LAMC2 knockdown in AMC-HN-8 cells had opposite effects. Furthermore, shLAMC2 decreased tumor volume and the expression of LAMC2, Ki-67 and integrinβ1, but increased the expression of E-cadherin in LSCC tumor-bearing mice. Conclusion The findings suggested that LAMC2 was overexpressed in LSCC and correlated with poor prognosis. LAMC2 knockdown inhibited LSCC progression by regulating the integrinβ1/FAK/Src/AKT signaling pathway. Therefore, LAMC2 could be a target for LSCC therapy.

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Overexpression of TEAD4 correlates with poor prognosis of glioma and promotes cell invasion.

Publications

Overexpression of TEAD4 correlates with poor prognosis of glioma and promotes cell invasion.

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