ReviewJournal of cell science2013
Mechanisms that link the oncogenic epithelial-mesenchymal transition to suppression of anoikis.
Review in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02402348 (Pilot Study of Metformin), which is not on this map. Cited by 184 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Pilot Study of Metformin (MF) IN HNSCC (Head and Neck Squamous Cell Carcinoma) as Window Trial Design in Operable HNSCC, to Investigate the Effects of MF, Tumor Genotype and MF Genotype Interactions, on Tumor Metabolism and Anoikis
Who cites it
184 citing papers in PubMed, 1 synthesis or guideline pooled it, 288 citations in OpenAlex.
- Prognostic Value of Focal Adhesion Kinase (FAK) in Human Solid Carcinomas: A Meta-Analysis.PloS one · 2016Pooled it
- New and emerging strategies for targeting cancers: Challenges and opportunities (Review).Oncology letters · 2026Review
- Interleukin 32 Expression in Mesothelioma.Thoracic cancer · 2026Article
- ITGA5 as a Dual Regulator of Epithelial-Mesenchymal Transition and Epithelial Cell Anoikis Resistance: Functional Validation and Drug Prediction.Cell proliferation · 2026Article
- Canonical and noncanonical Hippo signaling in C. elegans.Genetics · 2026Article
- Cathepsin L as a Driver of Tumour Invasion and a Novel Therapeutic Target in Ovarian Cancer.Cancers · 2026Review
- WWP1 gain-of-function drives developmental anoikis through TGFβ pathway during neurodevelopment.Cell death discovery · 2026Article
- Role and Mechanism ofInternational journal of molecular sciences · 2026Article
- Prognostic prediction and immune correlation analysis of anoikis- and epithelial-mesenchymal transition-related genes in lung adenocarcinoma.Translational cancer research · 2026Article
- Anoikis resistance and metastasis of ovarian cancer can be overcome by CDK8/19 mediator kinase inhibition.JCI insight · 2026Article
- Transforming growth factor-β and integrins: key players in EMT and breast cancer progression.Cancer cell international · 2026Review
- TGF-β in tumor development and progression: mechanisms and therapeutics.Molecular biomedicine · 2026Review
- Anoikis: To Die or Not to Die?International journal of molecular sciences · 2026Review
- HOXB5 in precision oncology: regulatory networks, functional duality, and clinical prospects.Journal of translational medicine · 2026Review
- Advancing Prognosis Prediction and Immunotherapy Efficacy in Lung Adenocarcinoma Through Machine Learning: Novel Insights From Anoikis Regulator Patterns in Single-Cell Multiomics.International journal of genomics · 2026Article
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- The involvement of circular RNAs in breast cancer metastasis: Insight into EMT-related signaling pathways.BioImpacts : BI · 2026Review
- Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism.Cancer research · 2025Article
- Unraveling the anoikis-cancer nexus: a bibliometric analysis of research trends and mechanisms.Future science OA · 2025Article
- The integrin-matrix-FAK-EMT axis in Anoikis resistance: a critical network in tumor progression and therapy.Molecular biology reports · 2025Review
124 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The oncogenic epithelial-mesenchymal transition (EMT) contributes to tumor progression in various context-dependent ways, including increased metastatic potential, expansion of cancer stem cell subpopulations, chemo-resistance and disease recurrence. One of the hallmarks of EMT is resistance of tumor cells to anoikis. This resistance contributes to metastasis and is a defining property not only of EMT but also of cancer stem cells. Here, we review the mechanistic coupling between EMT and resistance to anoikis. The discussion focuses on several key aspects. First, we provide an update on new pathways that lead from the loss of E-cadherin to anoikis resistance. We then discuss the relevance of transcription factors that are crucial in wound healing in the context of oncogenic EMT. Next, we explore the consequences of the breakdown of cell-polarity complexes upon anoikis sensitivity, through the Hippo, Wnt and transforming growth factor β (TGF-β) pathways, emphasizing points of crossregulation. Finally, we summarize the direct regulation of cell survival genes through EMT-inducing transcription factors, and the roles of the tyrosine kinases focal adhesion kinase (FAK) and TrkB neurotrophin receptor in EMT-related regulation of anoikis. Emerging from these studies are unifying principles that will lead to improvements in cancer therapy by reprogramming sensitivity of anoikis.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.