Faculty Opinions recommendation of Revisiting Epithelial-to-Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the "Reactive" Biliary Epithelial Phenotype.

2018 ◽  
Author(s):  
Shannon Glaser
Keyword(s):  
Liver Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Epithelial Phenotype

scholarly journals Controversies over the Epithelial-to-Mesenchymal Transition in Liver Fibrosis

2016 ◽  
Vol 5 (1) ◽  
pp. 9 ◽  
Author(s):  
Kojiro Taura ◽  
Keiko Iwaisako ◽  
Etsuro Hatano ◽  
Shinji Uemoto
Keyword(s):  
Liver Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Complete loss of miR-200 family induces EMT associated cellular senescence in gastric cancer

Oncogene ◽  
2021 ◽  
Author(s):  
Liang Yu ◽  
Can Cao ◽  
Xu Li ◽  
Mili Zhang ◽  
Qisheng Gu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Epithelial To Mesenchymal Transition ◽  
Micro Rna ◽  
Mesenchymal Transition ◽  
Morphological Alterations ◽  
Cellular Processes ◽  
Senescent Phenotype ◽  
Poor Treatment ◽  
Epithelial Phenotype ◽  
And Control

AbstractThe EMT (epithelial-to-mesenchymal-transition) subtype of gastric cancer (GC) is associated with poor treatment responses and unfavorable clinical outcomes. Despite the broad physiological roles of the micro-RNA (miR)-200 family, they largely serve to maintain the overall epithelial phenotype. However, during late-stage gastric tumorigenesis, members of the miR-200 family are markedly suppressed, resulting in the transition to the mesenchymal state and the acquisition of invasive properties. As such, the miR-200 family represents a robust molecular marker of EMT, and subsequently, disease severity and prognosis. Most reports have studied the effect of single miR-200 family member knockdown. Here, we employ a multiplex CRISPR/Cas9 system to generate a complete miR-200 family knockout (FKO) to investigate their collective and summative role in regulating key cellular processes during GC pathogenesis. Genetic deletion of all miR-200s in the human GC cell lines induced potent morphological alterations, G1/S cell cycle arrest, increased senescence-associated β-galactosidase (SA-β−Gal) activity, and aberrant metabolism, collectively resembling the senescent phenotype. Coupling RNA-seq data with publicly available datasets, we revealed a clear separation of senescent and non-senescent states amongst FKO cells and control cells, respectively. Further analysis identified key senescence-associated secretory phenotype (SASP) components in FKO cells and a positive feedback loop for maintenance of the senescent state controlled by activation of TGF-β and TNF-α pathways. Finally, we showed that miR-200 FKO associated senescence in cancer epithelial cells significantly recruited stromal cells in the tumor microenvironment. Our work has identified a new role of miR-200 family members which function as an integrated unit serving to link senescence with EMT, two major conserved biological processes.

scholarly journals Isoliquiritigenin Inhibits Ovarian Cancer Metastasis by Reversing Epithelial-to-Mesenchymal Transition

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3725 ◽  
Author(s):  
Chen Chen ◽  
Shuang Huang ◽  
Chang-Liang Chen ◽  
Sing-Bing Su ◽  
Dong-Dong Fang
Keyword(s):  
Ovarian Cancer ◽  
Cancer Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Tumor Development ◽  
Skov3 Cell ◽  
Anticancer Activities ◽  
Mesenchymal Transition ◽  
Epithelial Phenotype ◽  
Ovary Tumor

The epithelial-to-mesenchymal transition (EMT) plays a prominent role in cancer metastasis. Isoliquiritigenin (ISL), one of the flavonoids in licorice, has been shown to exhibit anticancer activities in many cancer types through various mechanisms. However, it is unknown whether ISL impacts the EMT process. Here, we show that ISL is able to suppress mesenchymal features of ovarian cancer SKOV3 and OVCAR5 cells, evidenced by an apparent morphological change from a mesenchymal to an epithelial phenotype and reduced levels of mesenchymal markers accompanied by the gain of E-cadherin expression. The suppression of EMT is also supported by the observed decrease in cell migration and in vitro invasion upon ISL treatment. Moreover, we show that ISL effectively blocks the intraperitoneal xenograft development of the SKOV3 cell line and prolonged the survival of tumor-bearing mice. These data suggest that ISL inhibits intraperitoneal ovary tumor development through the suppression of EMT, indicating that ISL may be an effective therapeutic agent against ovarian cancer.

scholarly journals Autoregulation of E-cadherin expression by cadherin–cadherin interactions

2003 ◽  
Vol 163 (4) ◽  
pp. 847-857 ◽  
Author(s):  
Maralice Conacci-Sorrell ◽  
Inbal Simcha ◽  
Tamar Ben-Yedidia ◽  
Janna Blechman ◽  
Pierre Savagner ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Epithelial To Mesenchymal Transition ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Mesenchymal Transition ◽  
Erk Activation ◽  
Epithelial Phenotype ◽  
Low Levels ◽  
Human Colon Cancer Cells ◽  
E Cadherin

Transcriptional repression of E-cadherin, characteristic of epithelial to mesenchymal transition, is often found also during tumor cell invasion. At metastases, migratory fibroblasts sometimes revert to an epithelial phenotype, by a process involving regulation of the E-cadherin–β-catenin complex. We investigated the molecular basis of this regulation, using human colon cancer cells with aberrantly activated β-catenin signaling. Sparse cultures mimicked invasive tumor cells, displaying low levels of E-cadherin due to transcriptional repression of E-cadherin by Slug. Slug was induced by β-catenin signaling and, independently, by ERK. Dense cultures resembled a differentiated epithelium with high levels of E-cadherin and β-catenin in adherens junctions. In such cells, β-catenin signaling, ErbB-1/2 levels, and ERK activation were reduced and Slug was undetectable. Disruption of E-cadherin–mediated contacts resulted in nuclear localization and signaling by β-catenin, induction of Slug and inhibition of E-cadherin transcription, without changes in ErbB-1/2 and ERK activation. This autoregulation of E-cadherin by cell–cell adhesion involving Slug, β-catenin and ERK could be important in tumorigenesis.

scholarly journals Fuzheng Huayu Recipe Ameliorates Liver Fibrosis by Restoring Balance between Epithelial-to-Mesenchymal Transition and Mesenchymal-to-Epithelial Transition in Hepatic Stellate Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Qin Pan ◽  
Yu-Qin Wang ◽  
Guang-Ming Li ◽  
Xiao-Yan Duan ◽  
Jian-Gao Fan
Keyword(s):  
Liver Fibrosis ◽  
P38 Mapk ◽  
Hepatic Stellate Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Stellate Cells ◽  
Cordyceps Sinensis ◽  
Dependent Manner ◽  
Radix Salviae Miltiorrhizae ◽  
Mesenchymal Transition ◽  
Mesenchymal To Epithelial Transition

Activation of hepatic stellate cells (HSCs) depending on epithelial-to-mesenchymal transition (EMT) reflects the key event of liver fibrosis. Contrastively, mesenchymal-to-epithelial transition (MET) of HSCs facilitates the fibrosis resolution. Here we investigated the effect of Fuzheng Huayu (FZHY) recipe, a Chinese herbal decoction made ofRadix Salviae Miltiorrhizae,Semen Persicae,Cordyceps sinensis,Pollen Pini, andGynostemma pentaphyllum, on liver fibrosis concerning the balance of EMT and MET in HSCs. In contrast to the increased TGF-β1/BMP-7 ratio in activated HSCs, FZHY administration induced significant upregulation of BMP-7 and downregulation of TGF-β1at both transcription and translation levels. Restoration of TGF-β1/BMP-7 ratio inhibited the expression of p38 MAPK and phosphorylated p38 MAPK, resulting in the reversal of epithelial-to-mesenchymal transition (EMT) to mesenchymal-to-epithelial transition (MET) as characterized by the abolishment of EMT markers (α-SMA and desmin) and reoccurrence of MET marker (E-cadherin).In vivotreatment of FZHY recipe also demonstrated the statistical reduction of activated HSCs with EMT phenotype, which attenuated the carbon tetrachloride- (CCl4-) induced liver fibrosis in a dose-dependent manner. These findings may highlight a novel antifibrotic role of FZHY recipe on the basis of rebalancing EMT and MET in HSCs.

scholarly journals Fibroblasts Derive from Hepatocytes in Liver Fibrosis via Epithelial to Mesenchymal Transition

2007 ◽  
Vol 282 (32) ◽  
pp. 23337-23347 ◽  
Author(s):  
Michael Zeisberg ◽  
Changqing Yang ◽  
Margot Martino ◽  
Michael B. Duncan ◽  
Florian Rieder ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition
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