New Insights into the Crossroads between EMT and Stemness in the Context of Cancer

Fabregat, Isabel; Malfettone, Andrea; Soukupová, Jitka

doi:10.3390/jcm5030037

Cited by 122 publications

(99 citation statements)

References 86 publications

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“…Stemness is also associated with EMT. In the procession of EMT in epithelial cells, the stem cell properties increased . Our study demonstrated that chronic ethanol exposure promoted stemness of HCC cells which was accompanied by enhanced with EMT.…”

Section: Discussionmentioning

confidence: 58%

Epithelial to mesenchymal transition is involved in ethanol promoted hepatocellular carcinoma cells metastasis and stemness

Chen

Wang

et al. 2018

Molecular Carcinogenesis

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Hepatocellular Carcinoma (HCC) is a malignant tumor with high rate of relapse and metastasis. Ethanol is a well‐known risk factor for HCC; it promotes the progression and aggressiveness of HCC. However, the underlying mechanism remains unclear. In clinic studies, we showed that alcohol consumption is positively correlated with TNM stage and vessel invasion; HCC patients with chronic drinking history had faster progression rate and poorer prognosis compared to non‐drinkers. In experimental models, ethanol exposure enhanced the metastasis, and invasion of HCC cells. Ethanol exposure increased cancer stem cells (CSC) population and enhanced stemness of HCC cells in vitro and in vivo. Mechanically, we found that ethanol exposure induced epithelial to mesenchymal transition (EMT) through activating Wnt/β‐catenin signaling pathway in HCC cells. We further demonstrated that β‐catenin siRNA or salinomycin (an inhibitor of Wnt/β‐catenin pathway) partially rescued ethanol‐induced EMT. In conclusion, this study suggested that ethanol exposure promotes the metastasis and stemness of HCC cells by inducing EMT.

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Section: Discussionmentioning

confidence: 58%

Epithelial to mesenchymal transition is involved in ethanol promoted hepatocellular carcinoma cells metastasis and stemness

Chen

Wang

et al. 2018

Molecular Carcinogenesis

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“…Third, activation of EMT in injury and many other situations is frequently associated with activation of genes typical of stem cell states, and increased stemness (Liao & Yang, ; reviewed in Fabregat, Malfettone, & Soukupova, ). Stemness is associated with loosened phenotypic restrictions and enhanced plasticity.…”

Section: Adaptive Cellular Reprogrammingmentioning

confidence: 99%

“…The EMT/stemness association is shown for instance by the findings that typical inducers of EMT, such as Snail, Slug, or TGFβ, also activate stem cell properties (Mani et al, ; Morel et al, ). A stem cell‐like phenotype is also induced by other EMT inducers, including Zeb and Twist (reviewed in Fabregat et al, ). In line with this, invasive tumor cells express both EMT and stemness characteristics (reviewed in Jordan, Johnson, & Abell, ; Rhim et al, .…”

Section: Adaptive Cellular Reprogrammingmentioning

confidence: 99%

Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves

Jessen

Arthur‐Farraj

2019

Glia

250

260

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Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. At the cellular level, many other tissues also react to injury by cellular reprogramming, generating cells specialized to promote tissue homeostasis and repair. And at the molecular level, a common feature possessed by Schwann cells and many other cells is the injury‐induced activation of genes associated with epithelial–mesenchymal transitions and stemness, differentiation states that are linked to cellular plasticity and that help injury‐induced tissue remodeling. The number of signaling systems regulating Schwann cell plasticity is rapidly increasing. Importantly, this includes mechanisms that are crucial for the generation of functional repair Schwann cells and nerve regeneration, although they have no or a minor role elsewhere in the Schwann cell lineage. This encourages the view that selective tools can be developed to control these particular cells, amplify their repair supportive functions and prevent their deterioration. In this review, we discuss the emerging similarities between the injury response seen in nerves and in other tissues and survey the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells, with emphasis on systems that selectively regulate the Schwann cell injury response.

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“…Aggressive tumor progression and poor therapeutic outcomes have been attributed to characteristic cellular plasticity due to abnormal elevation of EMT-TFs [41]. Expression of EMT-TFs is repressed in somatic tissues but reactivated during cancer development by a variety of cell-autonomous pathways and microenvironmental cues [50].…”

Section: Regulation Of Emt-tfsmentioning

confidence: 99%

Tackling Cancer Stem Cells via Inhibition of EMT Transcription Factors

Mladinich

Ruan

Chan

2016

Stem Cells International

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Cancer stem cell (CSC) has become recognized for its role in both tumorigenesis and poor patient prognosis in recent years. Traditional therapeutics are unable to effectively eliminate this group of cells from the bulk population of cancer cells, allowing CSCs to persist posttreatment and thus propagate into secondary tumors. The therapeutic potential of eliminating CSCs, to decrease tumor relapse, has created a demand for identifying mechanisms that directly target and eliminate cancer stem cells. Molecular profiling has shown that cancer cells and tumors that exhibit the CSC phenotype also express genes associated with the epithelial-to-mesenchymal transition (EMT) feature. Ample evidence has demonstrated that upregulation of master transcription factors (TFs) accounting for the EMT process such as Snail/Slug and Twist can reprogram cancer cells from differentiated to stem-like status. Despite being appealing therapeutic targets for tackling CSCs, pharmacological approaches that directly target EMT-TFs remain impossible. In this review, we will summarize recent advances in the regulation of Snail/Slug and Twist at transcriptional, translational, and posttranslational levels and discuss the clinical implication and application for EMT blockade as a promising strategy for CSC targeting.

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New Insights into the Crossroads between EMT and Stemness in the Context of Cancer

Cited by 122 publications

References 86 publications

Epithelial to mesenchymal transition is involved in ethanol promoted hepatocellular carcinoma cells metastasis and stemness

Epithelial to mesenchymal transition is involved in ethanol promoted hepatocellular carcinoma cells metastasis and stemness

Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves

Tackling Cancer Stem Cells via Inhibition of EMT Transcription Factors

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