ReviewFrontiers in pharmacology2018
How Tumor Cells Choose Between Epithelial-Mesenchymal Transition and Autophagy to Resist Stress-Therapeutic Implications.
Review in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Article
- Review
- A phase 1b, multicentre, dose escalation, safety and pharmacokinetics study of tilvestamab (BGB149) in relapsed, platinum-resistant, high-grade serous ovarian cancer (PROC) patients.British journal of cancer · 2025Article
- Oxidative and Glycolytic Metabolism: Their Reciprocal Regulation and Dysregulation in Cancer.Cells · 2025Review
- The role of glycolysis in tumorigenesis: From biological aspects to therapeutic opportunities.Neoplasia (New York, N.Y.) · 2024Review
- Review
- Identification of distinct slow mode of reversible adaptation of pancreatic ductal adenocarcinoma to the prolonged acidic pH microenvironment.Journal of experimental & clinical cancer research : CR · 2022Article
- Tumor Cell Glycolysis-At the Crossroad of Epithelial-Mesenchymal Transition and Autophagy.Cells · 2022Review
- CENP-A overexpression promotes distinct fates in human cells, depending on p53 status.Communications biology · 2021Article
- Epithelial-mesenchymal transition and metastasis of colon cancer cells induced by the FAK pathway in cancer-associated fibroblasts.The Journal of international medical research · 2020Article
- The Aberrant Expression of the Mesenchymal Variant of FGFR2 in the Epithelial Context Inhibits Autophagy.Cells · 2019Article
- The Vicious Cross-Talk between Tumor Cells with an EMT Phenotype and Cells of the Immune System.Cells · 2019Review
- Review
- From "high" ZEB1 to "low" B-cell lymphoma 2-interacting mediator of cell death (BIM)-an epithelial-mesenchymal transition (EMT)-associated drug resistance pathway elucidated.Journal of thoracic disease · 2019Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells undergo epithelial-mesenchymal transition (EMT) or macroautophagy (hereafter autophagy) in response to stressors from the microenvironment. EMT ensues when stressors act on tumor cells in the presence of nutrient sufficiency, and mechanistic target of rapamycin (mTOR) appears to be the crucial signaling node for EMT induction. Autophagy, on the other hand, is induced in the presence of nutrient deprivation and/or stressors from the microenvironment with 5' adenosine monophosphate-activated protein kinase (AMPK) playing an important, but not exclusive role, in autophagy induction. Importantly, mTOR and EMT on one hand, and AMPK and autophagy on the other hand, negatively regulate each other. Such regulation occurs at different levels and suggests that, in many instances, these two stress responses are mutually exclusive. Nevertheless, EMT and autophagy are able to interconvert and we suggest that this may depend on spatiotemporal changes in the tumor microenvironment and/or on duration/intensity of the stressor signal(s). Eventually, we propose a three-pronged therapeutic approach aimed at targeting these three major tumor cell populations. First, cytotoxic drugs that act on differentiated and proliferating tumor cells and which,
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