ArticleMolecular biology of the cell2021
Integrin-linked kinase tunes cell-cell and cell-matrix adhesions to regulate the switch between apoptosis and EMT downstream of TGFβ1.
Article in Molecular biology of the cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- The novel integrin-linked kinase inhibitor nilotinib suppresses cancer progression by promoting ubiquitylation of autoimmune regulator in oesophageal squamous cell carcinoma.Anti-cancer drugs · 2026Article
- Identification of a CSC-Associated miRNA Signature in NSCLC and Functional Characterization of hsa-let-7a-3p.Biomedicines · 2026Article
- The biomechanical signature of tumor invasion.Genes & diseases · 2026Review
- Neutrophil extracellular trap gene expression signatures identify prognostic and targetable signaling axes for inhibiting pancreatic tumour metastasis.Communications biology · 2025Article
- The role and regulation of integrins in cell migration and invasion.Nature reviews. Molecular cell biology · 2025Review
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Innovative Theranostics Strategies in the Fight Against Lung Cancer.Mini reviews in medicinal chemistry · 2025Review
- ECM-dependent regulation of septin 7 in focal adhesions promotes mechanosensing and functional response in fibroblasts.iScience · 2024Article
- Talin-1 variants associated with spontaneous coronary artery dissection (SCAD) highlight how even subtle changes in multi-functional scaffold proteins can manifest in disease.Human molecular genetics · 2024Article
- SPHK1 potentiates colorectal cancer progression and metastasis via regulating autophagy mediated by TRAF6-induced ULK1 ubiquitination.Cancer gene therapy · 2024Article
- Matrix Stiffness Regulated Endoplasmic Reticulum Stress-mediated Apoptosis of Osteosarcoma Cell through Ras Signal Cascades.Cell biochemistry and biophysics · 2023Article
- Mechanotransduction pathways in regulating epithelial-mesenchymal plasticity.Current opinion in cell biology · 2023Review
- Kallistatin Deficiency Induces the Oxidative Stress-Related Epithelial-Mesenchymal Transition of Retinal Pigment Epithelial Cells: A Novel Protagonist in Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2023Article
- Regulation of epithelial-mesenchymal transition by tumor microenvironmental signals and its implication in cancer therapeutics.Seminars in cancer biology · 2023Review
- High glucose induces an activated state of partial epithelial-mesenchymal transition in human primary tubular cell cultures.PloS one · 2023Article
- Epithelial-to-Mesenchymal Transition in Metastasis: Focus on Laryngeal Carcinoma.Biomedicines · 2022Review
- New Perspectives on the Role of Integrin-Linked Kinase (ILK) Signaling in Cancer Metastasis.Cancers · 2022Article
- The Expression of Proto-OncogeneInternational journal of molecular sciences · 2022Review
- Mapping phenotypic heterogeneity in melanoma onto the epithelial-hybrid-mesenchymal axis.Frontiers in oncology · 2022Article
- Substratum stiffness signals through integrin-linked kinase and β1-integrin to regulate midbody proteins and abscission during EMT.Molecular biology of the cell · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a morphogenetic process that endows epithelial cells with migratory and invasive potential. Mechanical and chemical signals from the tumor microenvironment can activate the EMT program, thereby permitting cancer cells to invade the surrounding stroma and disseminate to distant organs. Transforming growth factor β1 (TGFβ1) is a potent inducer of EMT that can also induce apoptosis depending on the microenvironmental context. In particular, stiff microenvironments promote EMT while softer ones promote apoptosis. Here, we investigated the molecular signaling downstream of matrix stiffness that regulates the phenotypic switch in response to TGFβ1 and uncovered a critical role for integrin-linked kinase (ILK). Specifically, depleting ILK from mammary epithelial cells precludes their ability to sense the stiffness of their microenvironment. In response to treatment with TGFβ1, ILK-depleted cells undergo apoptosis on both soft and stiff substrata. We found that knockdown of ILK decreases focal adhesions and increases cell-cell adhesions, thus shifting the balance from cell-matrix to cell-cell adhesion. High cell-matrix adhesion promotes EMT whereas high cell-cell adhesion promotes apoptosis downstream of TGFβ1. These results highlight an important role for ILK in controlling cell phenotype by regulating adhesive connections to the local microenvironment.
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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.