Epithelial-mesenchymal transition （EMT） is initially considered as a physiological phenomenon during the embryogenesis of mammals, as well as a basic biological event maintaining the stability of the vital body. Rec...Epithelial-mesenchymal transition （EMT） is initially considered as a physiological phenomenon during the embryogenesis of mammals, as well as a basic biological event maintaining the stability of the vital body. Recent researches indicated that EMT plays a critical role in various tumors progression, through which epithelial cancers invade and metastasize. The cell characteristics are changed during EMT, in which the cells lose cell-cell and cell-matrix interactions and apical polarity, reorganize their cytoskeleton, and become isolated, motile, as well as resistant to anoikis, then become spindle-shaped mesenchymal cells. This review lays emphasis on studying the cell morphogenesis, makers and molecular mechanism regulation about EMT, discussing the relationship between the EMT and the cancer development and metastasis.展开更多
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 remain...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 lucifer- ase reporter assay was employed to detect downstream targets of miR-200b. Transwell migration assays were used to detect CRC cell migration. Results Westem 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 knock- down on cell migration.展开更多
基金Supported by the grants from the Natural Science Foundation of China （No. 81000998） Natural Science Foundation of Hubei Province of China （No. 2007ABA248）
文摘Epithelial-mesenchymal transition （EMT） is initially considered as a physiological phenomenon during the embryogenesis of mammals, as well as a basic biological event maintaining the stability of the vital body. Recent researches indicated that EMT plays a critical role in various tumors progression, through which epithelial cancers invade and metastasize. The cell characteristics are changed during EMT, in which the cells lose cell-cell and cell-matrix interactions and apical polarity, reorganize their cytoskeleton, and become isolated, motile, as well as resistant to anoikis, then become spindle-shaped mesenchymal cells. This review lays emphasis on studying the cell morphogenesis, makers and molecular mechanism regulation about EMT, discussing the relationship between the EMT and the cancer development and metastasis.
文摘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 lucifer- ase reporter assay was employed to detect downstream targets of miR-200b. Transwell migration assays were used to detect CRC cell migration. Results Westem 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 knock- down on cell migration.
