| 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 |
| View Full Text View/Add Comment Download reader |
| KeyWord:miR-200b; colorectal cancer (CRC); metalloproteinase (MMP); epithelial-mesenchymal transition (EMT); cell migration |
|
| Hits: 6883 |
| Download times: 7357 |
| Abstract: |
| 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. |
| Close |