ArticleCell death & disease2024
c-Fos regulated by TMPO/ERK axis promotes 5-FU resistance via inducing NANOG transcription in colon cancer.
Article in Cell death & disease, 2024. 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, 30 citations in OpenAlex.
- Ubiquitin receptor-mediated, ubiquitin-independent targeted protein degradation via 26Science advances · 2026Article
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
- Early radiotherapy delays acquired gefitinib resistance in EGFR-mutant NSCLC by suppressing c-FOS-associated survival signaling.Respiratory research · 2026Article
- NHE7-Driven endoplasmic reticulum stress signaling transmission promotes malignant progression of endometrial cancer via c-Fos/PRSS1/ERP27 axis.Journal of experimental & clinical cancer research : CR · 2026Article
- FOS drives podocyte injury and renal fibrosis in diabetic kidney disease via direct Smad3 binding.Cellular and molecular life sciences : CMLS · 2026Article
- Germacrone suppresses renal cancer growth by regulating c-Fos-mediated lipid metabolism.Lipids in health and disease · 2026Article
- Multifaceted Attack Networks of Artemisinin in Reversing Chemoresistance in Colorectal Cancer.Molecules (Basel, Switzerland) · 2026Review
- Integrating dynamic modeling of signaling pathways with subject-specific transcriptomic data to assess breast cancer risk.PloS one · 2026Article
- Tetrabenazine-induced miR-34a-5p suppresses the tumorigenicity of radioresistant colorectal cancer by inhibiting M2 macrophage polarization.Cell communication and signaling : CCS · 2025Article
- Endometrial Mesenchymal Stem Cell-Derived Exosomal miR-4669 Promotes EMT in Adenomyosis by Inducing M2 Macrophage Polarization via the DUSP6/ERK Pathway.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- SF3A3 Drives Tumorigenesis in Endometrial Cancer by Enhancing c-FOS Expression and Represents a Potential Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular and phenotypic characterization of 5-FU resistant colorectal cancer cells: toward enrichment of cancer stem cells.Cancer cell international · 2025Article
- Lentinan suppresses the progression of neuroblastoma by inhibiting FOS-mediated transcription activation of VRK1 to stabilize p53 protein.Cell death discovery · 2025Article
- Advances in the relationship between AP-1 and tumorigenesis, development and therapy resistance.Discover oncology · 2025Review
- Sevoflurane pretreatment alleviates hypoxia-reoxygenation-induced myocardial cell injury by upregulating miR-21-5p.Frontiers in cardiovascular medicine · 2025Article
- Identification of CTSC-driven progression in ESCC by single-cell sequencing and experimental validation.Frontiers in immunology · 2025Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- Kinase-phosphatase balance in exercise adaptation: phosphorylation programs, PTM crosstalk, and actionable gaps.Frontiers in sports and active living · 2025Review
- Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression.Cancers · 2024Review
- TNF-α-Induced NF-κB Alter the Methylation Status of Some Stemness Genes in HT-29 Human Colon Cancer Cell.Advanced biomedical research · 2024Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Acquired drug resistance is one of the most common limitations for the clinical response of colon cancer to 5-Fluorouracil (5-FU)-based chemotherapy. The relevant molecular mechanisms might be diversity, but still not be elucidated clearly. In this study, we aimed to investigate the potential mechanisms of c-Fos, a subfamily of activator protein-1, in 5-FU chemoresistance. We determined that phosphorylated c-Fos promoted colon cancer cells resistance to 5-FU by facilitating the cancer stemness. Mechanically, 5-FU treatment induced autolysosome-dependent degradation of TMPO, which subsequently triggered ERK-mediated phosphorylation of c-Fos. Additionally, c-Fos was found to bind to the promoter of NANOG and phosphorylation of c-Fos at Ser 374 was required for its regulation of NANOG expression. NANOG ablation impaired c-Fos/p-c-Fos induced 5-FU resistance and stemness. Taken together, these findings revealed that TMPO-mediated phosphorylation of c-Fos conferred 5-FU resistance by regulating NANOG expression and promoting cell stemness in colon cancer cells. c-Fos could be as a therapeutic target for colon cancer.
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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.