scholarly journals Homeobox B7 accelerates the cancer progression of gastric carcinoma cells by promoting epithelial–mesenchymal transition (EMT) and activating Src–FAK pathway

2019 ◽  
Vol Volume 12 ◽  
pp. 3743-3751 ◽  
Author(s):  
Jianghong Wu ◽  
Ziwen Long ◽  
Hong Cai ◽  
Shengjia Yu ◽  
Xiaowen Liu
Keyword(s):  
Gastric Carcinoma ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition

scholarly journals Chronic TGF-β exposure drives stabilized EMT, tumor stemness, and cancer drug resistance with vulnerability to bitopic mTOR inhibition

2019 ◽  
Vol 12 (570) ◽  
pp. eaau8544 ◽  
Author(s):  
Yoko Katsuno ◽  
Dominique Stephan Meyer ◽  
Ziyang Zhang ◽  
Kevan M. Shokat ◽  
Rosemary J. Akhurst ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Progression ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Transforming Growth Factor Β ◽  
Carcinoma Cells ◽  
Cancer Drug ◽  
Mtor Inhibition ◽  
Mesenchymal Transition

Tumors comprise cancer stem cells (CSCs) and their heterogeneous progeny within a stromal microenvironment. In response to transforming growth factor–β (TGF-β), epithelial and carcinoma cells undergo a partial or complete epithelial-mesenchymal transition (EMT), which contributes to cancer progression. This process is seen as reversible because cells revert to an epithelial phenotype upon TGF-β removal. However, we found that prolonged TGF-β exposure, mimicking the state of in vivo carcinomas, promotes stable EMT in mammary epithelial and carcinoma cells, in contrast to the reversible EMT induced by a shorter exposure. The stabilized EMT was accompanied by stably enhanced stem cell generation and anticancer drug resistance. Furthermore, prolonged TGF-β exposure enhanced mammalian target of rapamycin (mTOR) signaling. A bitopic mTOR inhibitor repressed CSC generation, anchorage independence, cell survival, and chemoresistance and efficiently inhibited tumorigenesis in mice. These results reveal a role for mTOR in the stabilization of stemness and drug resistance of breast cancer cells and position mTOR inhibition as a treatment strategy to target CSCs.

scholarly journals ADAM17 promotes epithelial-mesenchymal transition via TGF-β/Smad pathway in gastric carcinoma cells

2016 ◽  
Vol 49 (6) ◽  
pp. 2520-2528 ◽  
Author(s):  
Min Xu ◽  
Hailang Zhou ◽  
Chunli Zhang ◽  
Junbo He ◽  
Hong Wei ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Smad Pathway ◽  
Mesenchymal Transition

scholarly journals Inhibition of MIR4435-2HG on Invasion, Migration, and EMT of Gastric Carcinoma Cells by Mediating MiR-138-5p/Sox4 Axis

2021 ◽  
Vol 11 ◽  
Author(s):  
Li-Fei Gao ◽  
Wei Li ◽  
Ya-Gang Liu ◽  
Cui Zhang ◽  
Wei-Na Gao ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Tumor Growth ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
The Cancer Genome Atlas ◽  
Cell Counting ◽  
Pcr Analysis ◽  
Mesenchymal Transition ◽  
Qrt Pcr

BackgroundThe previous investigations have identified that long non-coding RNA (lncRNAs) act as crucial regulators in gastric carcinoma. However, the function of lncRNA MIR4435-2HG in the modulation of gastric carcinoma remains elusive. Here, we aimed to explore the role of MIR4435-2HG in gastric carcinoma.MethodThe Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were applied to select the differently expressed lncRNAs in gastric carcinoma. The qRT-PCR was applied to analyze MIR4435-2HG expression in carcinoma tissues and cell lines. The effect of MIR4435-2HG on proliferation, invasion, migration, and apoptosis of gastric carcinoma cells was detected by Cell Counting Kit-8 (CCK-8) assays, transwell assays, and flow cytometry in vitro. A subcutaneous tumor model was constructed to examine the tumor growth of gastric carcinoma cells after knocking out MIR4435-2HG. RNA immunoprecipitation and luciferase reporting assays were applied to evaluate the interaction of MIR4435-2HG, miR-138-5p, and Sox4.ResultsThe bioinformatics analysis based on TCGA and GEO databases indicated that MIR4435-2HG was obviously elevated in gastric carcinoma samples. The qRT-PCR analysis revealed that MIR4435-2HG was upregulated in clinical gastric carcinoma tissues and cells. The high expression of MIR4435-2HG is associated with the poor survival rate of patients. The knockout of MIR4435-2HG could repress the proliferation, invasion, migration, and epithelial–mesenchymal transition (EMT) and accelerate the apoptosis of gastric carcinoma cells. Moreover, the deletion of MIR4435-2HG was able to attenuate the tumor growth in vivo. Mechanically, we identified that MIR4435-2HG enhanced Sox4 expression by directly interacting with miR-138-5p as a competitive endogenous RNA (ceRNA) in gastric carcinoma cells, in which Sox4 was targeted by miR-138-5p.ConclusionMIR4435-2HG is elevated in gastric carcinoma cells and contributes to the growth, metastasis, and EMT of gastric carcinoma cells by targeting miR-138-5p/Sox4 axis. MIR4435-2HG may be applied as a potential therapeutic target in gastric carcinoma.

Radiofrequency ablation triggers the migration of hepatocellular carcinoma cells by suppressing miR-148a-5p

2020 ◽  
Vol 401 (8) ◽  
pp. 985-994
Author(s):  
Haicun Wang ◽  
Yang Cao ◽  
Kaiwen Hu ◽  
Quanwang Li ◽  
Yufei Yang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Radiofrequency Ablation ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Ataxia Telangiectasia Mutated ◽  
Mesenchymal Transition ◽  
Insufficient Radiofrequency Ablation ◽  
Hcc Cells

AbstractIncreasing evidences suggest that insufficient radiofrequency ablation (IRFA) can paradoxically promote tumor invasion and metastatic processes, whereas the effects of moderate hyperthermia on cancer progression are not well illustrated. Our study found that IRFA can increase the in vitro migration, invasion, and epithelial–mesenchymal transition (EMT) of hepatocellular carcinoma (HCC) cells via induction of Snail, a master regulator of EMT events. Among measured miRNAs, IRFA can decrease the expression of miR-148a-5p in HCC cells. Whereas overexpression of miR-148a-5p can reverse IRFA-induced migration of HCC cells and upregulation of Snail, mechanistically overexpression of miR-148a-5p can directly target and decrease the expression of protein kinase ATM (ataxia telangiectasia mutated), which can increase protein stability of Snail. Collectively, our data suggest that IRFA can regulate the miR-148a-5p/ATM/Snail axis to trigger migration of HCC cells.

Targeting epithelial–mesenchymal plasticity in cancer: clinical and preclinical advances in therapy and monitoring

2017 ◽  
Vol 474 (19) ◽  
pp. 3269-3306 ◽  
Author(s):  
Sugandha Bhatia ◽  
James Monkman ◽  
Alan Kie Leong Toh ◽  
Shivashankar H. Nagaraj ◽  
Erik W. Thompson
Keyword(s):  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Therapy Resistance ◽  
Carcinoma Cells ◽  
Related Phenomenon ◽  
Mesenchymal Transition ◽  
Control Loops ◽  
Monitoring Strategies ◽  
The Impact ◽  
Ability To Drive

The concept of epithelial–mesenchymal plasticity (EMP), which describes the dynamic flux within the spectrum of phenotypic states that invasive carcinoma cells may reside, is being increasingly recognised for its role in cancer progression and therapy resistance. The myriad of events that are able to induce EMP, as well as the more recently characterised control loops, results in dynamic transitions of cancerous epithelial cells to more mesenchymal-like phenotypes through an epithelial–mesenchymal transition (EMT), as well as the reverse transition from mesenchymal phenotypes to an epithelial one. The significance of EMP, in its ability to drive local invasion, generate cancer stem cells and facilitate metastasis by the dissemination of circulating tumour cells (CTCs), highlights its importance as a targetable programme to combat cancer morbidity and mortality. The focus of this review is to consolidate the existing knowledge on the strategies currently in development to combat cancer progression via inhibition of specific facets of EMP. The prevalence of relapse due to therapy resistance and metastatic propensity that EMP endows should be considered when designing therapy regimes, and such therapies should synergise with existing chemotherapeutics to benefit efficacy. To further improve upon EMP-targeted therapies, it is imperative to devise monitoring strategies to assess the impact of such treatments on EMP-related phenomenon such as CTC burden, chemosensitivity/-resistance and micrometastasis in patients.

scholarly journals miRNA-223 inhibits epithelial-mesenchymal transition in gastric carcinoma cells via Sp1

2016 ◽  
Vol 49 (1) ◽  
pp. 325-335 ◽  
Author(s):  
JING HU ◽  
ZHIYAN SHAN ◽  
KEWEI HU ◽  
FENGYUN REN ◽  
WEI ZHANG ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Mesenchymal Transition
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