scholarly journals PEG10 is imperative for TGF-β1-induced epithelial-mesenchymal transition in hepatocellular carcinoma

2016 ◽  
Vol 37 (1) ◽  
pp. 510-518 ◽  
Author(s):  
Minfeng Zhang ◽  
Chengjun Sui ◽  
Binghua Dai ◽  
Weifeng Shen ◽  
Jiongjiong Lu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tgf Β1

scholarly journals The Effect of Alpha Mangostin on Epithelial-Mesenchymal Transition on Human Hepatocellular Carcinoma HepG2 Cells Surviving Sorafenib via TGF-β/Smad Pathways

2020 ◽  
Vol 10 (4) ◽  
pp. 648-655
Author(s):  
Syarinta Adenina ◽  
Melva Louisa ◽  
Vivian Soetikno ◽  
Wawaimuli Arozal ◽  
Septelia Inawati Wanandi
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Sorafenib Treatment ◽  
Mesenchymal Transition ◽  
The Impact ◽  
Tgf Β1 ◽  
E Cadherin

Purpose : This study was intended to find out the impact of alpha mangostin administration on the epithelial-mesenchymal transition (EMT) markers and TGF-β/Smad pathways in hepatocellular carcinoma Hep-G2 cells surviving sorafenib. Methods: Hepatocellular carcinoma HepG2 cells were treated with sorafenib 10 μM. Cells surviving sorafenib treatment (HepG2surv) were then treated vehicle, sorafenib, alpha mangostin, or combination of sorafenib and alpha mangostin. Afterward, cells were observed for their morphology with an inverted microscope and counted for cell viability. The concentrations of transforming growth factor (TGF)-β1 in a culture medium were examined using ELISA. The mRNA expressions of TGF-β1, TGF-β1-receptor, Smad3, Smad7, E-cadherin, and vimentin were evaluated using quantitative reverse transcriptase–polymerase chain reaction. The protein level of E-cadherin was also determined using western blot analysis. Results: Treatment of alpha mangostin and sorafenib caused a significant decrease in the viability of sorafenib-surviving HepG2 cells versus control (both groups with P<0.05). Our study found that alpha mangostin treatment increased the expressions of vimentin (P<0.001 versus control). In contrast, alpha mangostin treatment tends to decrease the expressions of Smad7 and E-cadherin (both with P>0.05). In line with our findings, the expressions of TGF-β1 and Smad3 are significantly upregulated after alpha mangostin administration (both with P<0.05) versus control. Conclusion: Alpha mangostin reduced cell viability of sorafenib-surviving HepG2 cells; however, it also enhanced epithelial–mesenchymal transition markers by activating TGF-β/Smad pathways.

scholarly journals MicroRNA-199b-5p attenuates TGF-β1-induced epithelial–mesenchymal transition in hepatocellular carcinoma

2017 ◽  
Vol 117 (2) ◽  
pp. 233-244 ◽  
Author(s):  
Shao-jun Zhou ◽  
Fu-yao Liu ◽  
An-hong Zhang ◽  
Hui-fang Liang ◽  
Ye Wang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tgf Β1

scholarly journals GP73 promotes epithelial–mesenchymal transition and invasion partly by activating TGF-β1/Smad2 signaling in hepatocellular carcinoma

2018 ◽  
Vol 39 (7) ◽  
pp. 900-910 ◽  
Author(s):  
Ying Yang ◽  
Qiang Liu ◽  
Zhipeng Li ◽  
Ruili Zhang ◽  
Chunli Jia ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tgf Β1

scholarly journals Comment on ‘MicroRNA-199b-5p attenuates TGF-β1-induced epithelial–mesenchymal transition in hepatocellular carcinoma’

2018 ◽  
Vol 118 (7) ◽  
pp. 1028-1029 ◽  
Author(s):  
Ion Cristóbal ◽  
Andrea Santos ◽  
Silvia González ◽  
Melania Luque ◽  
Blanca Torrejón ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tgf Β1

scholarly journals TGF-β1 Induced Deficiency of Linc00261 Promotes Epithelial-mesenchymal-transition and Stemness of Hepatocellular Carcinoma via Modulating SMAD3

2021 ◽  
Author(s):  
Zhanjun Chen ◽  
Leyang Xiang ◽  
Huohui Ou ◽  
Yinghao Fang ◽  
Yuyan Xu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Tumor Sphere ◽  
Non Coding Rnas ◽  
Tgf Β1 ◽  
Hcc Cells

Abstract Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC).Kinds of lncRNAs were found to be involved in regulating epithelial-mesenchymal transition (EMT) or stem-like traits in human cancers, however, the molecular mechanism and signaling pathways targeting EMT and stemness remains largely unknown. Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinic pathological parameters and poor prognosis. Here, we show that linc00261 was down-regulated in TGF-β1 stimulated cells, and forced expression of linc00261 attenuated EMT and stem-like traits in HCC.Linc00261 also inhibited the tumor sphere forming in vitro and decreased the tumorigenicity in vivo. Furthermore, we revealed that linc00261 suppressed the expression and phosphorylation of SMAD3 (p-SMAD3), which is a core transcriptional modulator in TGF-β1 signaling mediated EMT and the acquisition of stemness traits. A negative correlation between linc00261 and p-SMAD3 was determined in HCC samples.Conclusion: Our study revealed that linc00261suppressed EMT and stem-like traits of HCC cells by inhibiting TGF-β1/SMAD3 signaling.

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