scholarly journals MicroRNA-145 Inhibits Cell Migration and Invasion and Regulates Epithelial-Mesenchymal Transition (EMT) by Targeting Connective Tissue Growth Factor (CTGF) in Esophageal Squamous Cell Carcinoma

2016 ◽  
Vol 22 ◽  
pp. 3925-3934 ◽  
Author(s):  
Qiang Han ◽  
Hua-Yong Zhang ◽  
Bei-Long Zhong ◽  
Xiao-Jing Wang ◽  
Bing Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Growth Factor ◽  
Connective Tissue ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Tissue Growth ◽  
Migration And Invasion ◽  
Mesenchymal Transition

scholarly journals MicroRNA-138 suppresses epithelial–mesenchymal transition in squamous cell carcinoma cell lines

2011 ◽  
Vol 440 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Xiqiang Liu ◽  
Cheng Wang ◽  
Zujian Chen ◽  
Yi Jin ◽  
Yun Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Migration ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Mesenchymal Transition ◽  
Cell Migration And Invasion ◽  
Direct Targeting

Down-regulation of miR-138 (microRNA-138) has been frequently observed in various cancers, including HNSCC (head and neck squamous cell carcinoma). Our previous studies suggest that down-regulation of miR-138 is associated with mesenchymal-like cell morphology and enhanced cell migration and invasion. In the present study, we demonstrated that these miR-138-induced changes were accompanied by marked reduction in E-cad (E-cadherin) expression and enhanced Vim (vimentin) expression, characteristics of EMT (epithelial–mesenchymal transition). On the basis of a combined experimental and bioinformatics analysis, we identified a number of miR-138 target genes that are associated with EMT, including VIM, ZEB2 (zinc finger E-box-binding homeobox 2) and EZH2 (enhancer of zeste homologue 2). Direct targeting of miR-138 to specific sequences located in the mRNAs of the VIM, ZEB2 and EZH2 genes was confirmed using luciferase reporter gene assays. Our functional analyses (knock-in and knock-down) demonstrated that miR-138 regulates the EMT via three distinct pathways: (i) direct targeting of VIM mRNA and controlling the expression of VIM at a post-transcriptional level, (ii) targeting the transcriptional repressors (ZEB2) which in turn regulating the transcription activity of the E-cad gene, and (iii) targeting the epigenetic regulator EZH2 which in turn modulates its gene silencing effects on the downstream genes including E-cad. These results, together with our previously observed miR-138 effects on cell migration and invasion through targeting RhoC (Rho-related GTP-binding protein C) and ROCK2 (Rho-associated, coiled-coil-containing protein kinase 2) concurrently, suggest that miR-138 is a multi-functional molecular regulator and plays major roles in EMT and in HNSCC progression.

scholarly journals Capsaicin Inhibits Migration and Invasion via Inhibiting Epithelial-Mesenchymal Transition in Esophageal Squamous Cell Carcinoma By Up-Regulation of Cldn3 Expression

2021 ◽  
Author(s):  
Ji Feng ◽  
Yin Xu ◽  
Zhouling Wei ◽  
Yiju Xia ◽  
Haoxiang Zhang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Lung Metastasis ◽  
Squamous Cell ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Positive Expression

Abstract Purpose To investigate the effects of capsaicin on migration and invasion of esophageal squamous cell carcinoma and the roles of claudin-3 and epithelial-mesenchymal transition (EMT).Methods Cldn3 expression was detected in paired cancerous and adjacent normal esophageal tissues by IHC. The association of Cldn3 with clinical data was analyzed. The migration and invasion of ESCC cells were investigated by exposure of capsaicin. The migration and invasion of ESCC cells with Cldn3 silencing or Cldn3 overexpression were also evaluated. The effects of capsaicin on lung metastasis of ESCC with or without Cldn3 silencing were evaluated.Results: The positive expression of Cldn3 was associated with better prognosis of ESCC patients. Capsaicin attenuated migration and invasion of ESCC and inhibited EMT in a dose-dependent manner. Cldn3 silencing enhanced migration and invasion and EMT in ESCC cells. Cldn3 overexpression inhibited migration and invasion and EMT, similar to exposure of capsaicin. Cldn3 silencing also attenuated inhibition of migration and invasion and EMT by exposure of capsaicin. Cldn3 silencing attenuated inhibition of lung metastasis of ESCC by exposure of capsaicin in vivo.Conclusion The positive expression of Cldn3 showed a better prognosis of ESCC, which was a potentially prognostic indicator. Capsaicin inhibited migration and invasion of ESCC through up-regulation of Cldn3 and inhibition of EMT.

Matrix Metalloproteinase (MMP)-12 Promote Invasion and Migration of Esophageal Squamous Cell Carcinoma Cell by Epithelial-Mesenchymal Transition

2019 ◽  
Vol 9 (8) ◽  
pp. 1120-1126
Author(s):  
Dong-Hui Shi ◽  
Jiang Jin
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Matrix Metalloproteinase ◽  
Cell Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Over Expression ◽  
And Migration

The present study aimed to investigate the role of matrix metalloproteinase (MMP)-12 on cell migration and invasion of esophageal squamous cell carcinoma (ESCC) though epithelial-mesenchymal transition (EMT). The ESCC cell lines (ECA-109, KYSE-30, KYSE-410, KYSE-520) and normal esophageal epithelial cells (HEEC) were cultured. ECA-109 cells were then chosen to be transfected with the plasmids of MMP-12 over-expression, MMP-12 inhibitor, E-cad over-expression and empty control vectors. The protein and mRNA levels of MMP-12 were detected using western blot and qRT-PCR analysis. Transwell and wound healing assays were used to assess cell invasion and migration. Results indicated that MMP-12 was upregulated significantly in all the ESCC cell lines. Overexpression of MMP-12 increased MMP-12 expression, and the abilities of invasion and migration of ECA-109 cells. Overexpression of MMP-12 increased the expression of N-cad and vimentin, but decreased E-cad expression. Additionally, we found that cells treated with inhibitor-MMP-12 were opposite to the above results. Moreover, up-regulation of E-cad were eliminated all effects on ECA-109 cells caused by MMP-12 over-expression. In conclusion, MMP-12 promoted ECA-109 cells migration and invasion by the alteration of the EMT marker protein, which is one of its mechanisms. Therefore, MMP-12 may be a new therapeutic target for ESCC.

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