miR-129-5p attenuates cell proliferation and epithelial mesenchymal transition via HMGB1 in gastric cancer

The miR-129-5p has been reported to be aberrant expression and exert vital roles in tumor progression of various malignancies. However, the effects on EMT in gastric cancer and its precise molecular mechanism in gastric cancer remain unclear. RT-qPCR was performed to evaluate the expression level of...

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Veröffentlicht in:Pathology, research and practice research and practice, 2019-04, Vol.215 (4), p.676-682
Hauptverfasser: Wang, Shaocheng, Chen, Yanyan, Yu, Xiongfei, Lu, Yimin, Wang, Haoao, Wu, Fusheng, Teng, Lisong
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container_issue 4
container_start_page 676
container_title Pathology, research and practice
container_volume 215
creator Wang, Shaocheng
Chen, Yanyan
Yu, Xiongfei
Lu, Yimin
Wang, Haoao
Wu, Fusheng
Teng, Lisong
description The miR-129-5p has been reported to be aberrant expression and exert vital roles in tumor progression of various malignancies. However, the effects on EMT in gastric cancer and its precise molecular mechanism in gastric cancer remain unclear. RT-qPCR was performed to evaluate the expression level of miR-129-5p and HMGB1 in cell lines. Cell proliferation was detected via CCK-8. The epithelial mesenchymal transition (EMT) related proteins and the expression of HMGB1 were detected by western blot analysis. Luciferase assays were used to validate binding seeds between miR-129-5p and HMGB1. miR-129-5p was downregulated in gastric cancer cells compared with GES-1. At the same time EMT was promoted in gastric cancer cells compared to GES-1. Overexpression of miR-129-5p inhibited EMT and proliferation. MiR-129-5p negatively and directly targeted HMGB1. HMGB1 was upregulated in gastric cancer cells and HMGB1 knocked-down inhibited EMT and cell proliferation. Taken together, upregulation of miR-129-5p associated with gastric cancer proliferation and EMT, and serves as a potential diagnostic and therapeutic target via miR-129-5p/HMGB1 pathway in gastric cancer.
doi_str_mv 10.1016/j.prp.2018.12.024
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However, the effects on EMT in gastric cancer and its precise molecular mechanism in gastric cancer remain unclear. RT-qPCR was performed to evaluate the expression level of miR-129-5p and HMGB1 in cell lines. Cell proliferation was detected via CCK-8. The epithelial mesenchymal transition (EMT) related proteins and the expression of HMGB1 were detected by western blot analysis. Luciferase assays were used to validate binding seeds between miR-129-5p and HMGB1. miR-129-5p was downregulated in gastric cancer cells compared with GES-1. At the same time EMT was promoted in gastric cancer cells compared to GES-1. Overexpression of miR-129-5p inhibited EMT and proliferation. MiR-129-5p negatively and directly targeted HMGB1. HMGB1 was upregulated in gastric cancer cells and HMGB1 knocked-down inhibited EMT and cell proliferation. 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However, the effects on EMT in gastric cancer and its precise molecular mechanism in gastric cancer remain unclear. RT-qPCR was performed to evaluate the expression level of miR-129-5p and HMGB1 in cell lines. Cell proliferation was detected via CCK-8. The epithelial mesenchymal transition (EMT) related proteins and the expression of HMGB1 were detected by western blot analysis. Luciferase assays were used to validate binding seeds between miR-129-5p and HMGB1. miR-129-5p was downregulated in gastric cancer cells compared with GES-1. At the same time EMT was promoted in gastric cancer cells compared to GES-1. Overexpression of miR-129-5p inhibited EMT and proliferation. MiR-129-5p negatively and directly targeted HMGB1. HMGB1 was upregulated in gastric cancer cells and HMGB1 knocked-down inhibited EMT and cell proliferation. 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subjects Epithelial mesenchymal transition
Gastric cancer
HMGB1
miR-129-5p
Proliferation
title miR-129-5p attenuates cell proliferation and epithelial mesenchymal transition via HMGB1 in gastric cancer
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