ArticleiScience2025
Stiff extracellular matrix activates the transcription factor ATF5 to promote the proliferation of cancer cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Article
- The potential of ATF5 as a prognostic marker and therapeutic target in cancer: insights from bioinformatics analysis and experimental validation.Translational cancer research · 2026Article
- Compressive stress inhibits proliferation in AsPC-1 pancreatic cancer cells and reduction of Myc protein.PloS one · 2026Article
- Chlorogenic acid promotes mtDNA leakage to enhance cGAS-STING induced anti-tumor immunity via ATF5-mtHSP70-TFAM system.International journal of biological sciences · 2026Article
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer tissues are stiffer than normal tissues. Carcinogenesis stiffens the extracellular matrix (ECM) of cancerous tissues, to which cancer cells respond by activating transcription factors, such as YAP/TAZ, Twist1, and β-catenin, which further elevate their malignancy. However, these transcription factors are also expressed in normal tissues. Therefore, inhibiting these factors in order to treat cancer may lead to severe side effects. Here, we show that activating transcription factor 5 (ATF5), highly expressed in tumors, is activated by ECM stiffness and promotes the proliferation of cancer cells, including that of pancreatic cancer cells and lung cancer cells. In addition, ATF5 suppressed the expression of early growth response 1 (EGR1), thereby accelerating cancer cell proliferation. Stiff ECMs trigger the JAK-MYC pathway which activates ATF5. JAK activation was actomyosin independent whereas MYC induction was actomyosin dependent. These results demonstrate the critical role played by ATF5 in the mechanotransduction process seen in cancers.
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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.