scholarly journals Significance of the hedgehog pathway-associated proteins Gli-1 and Gli-2 and the epithelial-mesenchymal transition-associated proteins Twist and E-cadherin in hepatocellular carcinoma

2016 ◽  
Vol 12 (3) ◽  
pp. 1753-1762 ◽  
Author(s):  
Hyung Wook Chun ◽  
Ran Hong
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Hedgehog Pathway ◽  
Mesenchymal Transition ◽  
Associated Proteins ◽  
Gli 1 ◽  
E Cadherin

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 RETRACTED ARTICLE: Correlations between chromobox homolog 8 and key factors of epithelial–mesenchymal transition in hepatocellular carcinoma

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiaonian Zhu ◽  
Wei Luo ◽  
Chunhua Bei ◽  
Juan Kong ◽  
Shidong Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
Knock Down ◽  
Retracted Article ◽  
Associated Proteins ◽  
And Migration ◽  
Hcc Cells

Abstract Background Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide, especially in China, with high metastasis and poor prognosis. Recently, as the core component of the polycomb repressive complexes 1 (PRC1), chromobox protein homolog 8 (CBX8) is considered as an oncogene and prognostic marker in HCC. Methods A tissue microarray of 166 paired HCC and adjacent non-tumor samples were collected to identify the relationship between CBX8 and epithelial mesenchymal transition (EMT) associated proteins by Spearman correlation analysis. Knock-down of CBX8 in HCC cells was conducted to detect the biologic functions of CBX8 in HCC metastasis. Results We found out that CBX8 was over-expressed in HCC and its expression was closely related to the metastasis of HCC patients. In addition, knock-down of CBX8 was found to inhibit the invasion and migration ability of HCC cells. Moreover, there was a significant relationship between expression of CBX8 and EMT associated proteins both in HCC cells and tumor tissues. Conclusions Our results indicate that CBX8 promotes metastasis of HCC by inducing EMT process.

scholarly journals Downregulation of UBAP2L Inhibits the Epithelial-Mesenchymal Transition via SNAIL1 Regulation in Hepatocellular Carcinoma Cells

2017 ◽  
Vol 41 (4) ◽  
pp. 1584-1595 ◽  
Author(s):  
Tao Ye ◽  
Jing Xu ◽  
Ling Du ◽  
Wenhui Mo ◽  
Yiming Liang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Western Blot ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Critical Role ◽  
Migration And Invasion ◽  
Biological Traits ◽  
Mesenchymal Transition ◽  
Qrt Pcr ◽  
E Cadherin

Background/Aims: Dysregulation of ubiquitin-associated protein 2-like (UBAP2L) has been reported in tumors, but its role in hepatocellular carcinoma (HCC) progression is unclear. Methods: The expression levels of UBAP2L in HCC tissues and HCC cell lines were detected by western blot and quantitative real-time (qRT) PCR. The effects of UBAP2L expression on HCC cell biological traits, including migration and invasion, were investigated by wound healing assay and matrigel transwell assay. Simultaneously, the expression of epithelial-mesenchymal transition (EMT) markers including E-cadherin, CK-18, N-cadherin, Vimentin, Claudin7 and the promoter activity of E-cadherin were detected by western blot and qRT-PCR. Subsequently, role of SNAIL1 in UBAP2L-mediated EMT and the mechanism underlying UBAP2L-mediated SNAIL1 expression were further investigated. Results: UBAP2L was overexpressed in human HCC tissues compared with peri-tumoral tissues. Downregulation of UBAP2L inhibited migration, invasion and the EMT in highly metastatic HCC cell lines. Furthermore, UBAP2L knockdown inhibited expression of the transcriptional repressor SNAIL1 and its ability to bind to the E-cadherin promoter via SMAD2 signaling pathway, which in turn resulted in increased E-cadherin expression. Additionally, bioinformatics analysis showed that expression of UBAP2L is correlated with poor prognosis in patients with HCC. Conclusions: UBAP2L plays a critical role in maintenance of the metastatic ability of HCC cells via SNAIL1 Regulation and is predictive of a poor clinical outcome.

scholarly journals Correction to: PHF8 upregulation contributes to autophagic degradation of E-cadherin, epithelial-mesenchymal transition and metastasis in hepatocellular carcinoma

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Wuhua Zhou ◽  
Li Gong ◽  
Qinchuan Wu ◽  
Chunyang Xing ◽  
Bajin Wei ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Autophagic Degradation ◽  
E Cadherin

In the publication of our publication [1], we have noticed there is a wrong label in Fig. 1e, in which the position of “HCC” and “Adjacent” should be transposed.

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