Gantao Chen,Yanxiang Cheng,Xiao Yang,Liu Yaodan,Weiguo Dong. Targeting of RhoE inhibits epithelial-mesenchymal transition during colorectal cancer cell migration. Oncol Transl Med, 2016, 2: 119-126.
Targeting of RhoE inhibits epithelial-mesenchymal transition during colorectal cancer cell migration
Received:December 14, 2015  Revised:June 10, 2016
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KeyWord:miR-200b; colorectal cancer (CRC); metalloproteinase (MMP); epithelial-mesenchymal transition (EMT); cell migration
Author NameAffiliationE-mail
Gantao Chen Renmin Hospital of Wuhan University 
Yanxiang Cheng Renmin Hospital of Wuhan University 
Xiao Yang Renmin Hospital of Wuhan University 
Liu Yaodan Renmin hospital of Wuhan University 
Weiguo Dong Renmin Hospital of Wuhan University 
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      Objective: Despite microRNA (miR-200b) being proved to promote the proliferation of colorectal cancer (CRC) cells, the relationship between miR-200b and epithelial-mesenchymal transition (EMT) of CRC cells remains poorly understood. The aim of the study was to investigate the relationship between miR-200b and EMT during CRC cell migration. Methods: The effect of miR-200b on EMT-associated markers E-cadherin and vimentin was evaluated by western blot in CRC cells (SW620 and HT-29) by treatment with miR-200b mimics and inhibitors. A luciferase reporter assay was employed to detect downstream targets of miR-200b. Transwell migration assays were used to detect CRC cell migration. Results: Western blots revealed that treatment with miR-200b mimics led to up-regulation of E-cadherin and down-regulation of vimentin, metalloproteinase (MMP)-9, and MMP-2, whereas treatment with miR- 200b inhibitor exhibited opposite effects on expression of E-cadherin and vimentin. Luciferase reporter assays demonstrated that RhoE (RND3) was targeted by miR-200b. Two predicted target sites of miR-200b were present in the 3’-UTR of RhoE. Predicted target site 1 was from nucleotides 1584 to 1591, and site 2 was from nucleotides 1729 to 1735. RhoE knockdown cell lines were also established to investigate the impact of RhoE and miR-200b on EMT and cell migration. RhoE knockdown enhanced the effect of miR- 200b mimics, up-regulating E-cadherin and down-regulating vimentin. RhoE knockdown also inhibited cell migration. Furthermore, miR-200b mimic treatment further promoted the inhibitory effect of RhoE knockdown on cell migration. Conclusion: miR-200b inhibited EMT and CRC cell migration partly via inhibiting RhoE expression in CRC. RhoE and miR-200b might therefore be promising target genes in the management of CRC.