ArticleCell death & disease2022
Nanog mediated by FAO/ACLY signaling induces cellular dormancy in colorectal cancer cells.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
- IL-24 Induces Cell Dormancy and Oxaliplatin Resistance in Colon Cancer Cells by Activating NF-κB Pathway.Molecular carcinogenesis · 2026Article
- Intracellular lipid droplets positively regulate the dormancy of colorectal cancer cells depending on ELF1-ACSL5 signaling.Journal of experimental & clinical cancer research : CR · 2026Article
- Combined Analysis of Bulk and Single-Cell Transcriptomic Data Reveals Dormancy-Associated Genes in Colorectal Cancer.International journal of molecular sciences · 2026Article
- Decoding the metabolic cipher of dormant cancer cells: molecular mechanisms and therapeutic potentials.Cell communication and signaling : CCS · 2026Review
- Ubiquitination of DDX21 by HERC2 induces a dormancy-like phenotype via the NUCKS1-p21/p27 axis to promote radio-resistance in colorectal cancer cells.Cell death & disease · 2026Article
- Regulating the dormancy of cancer stem cells: a novel approach to preventing cancer relapse.Cell death & disease · 2026Review
- Dormancy in Metastatic Colorectal Cancer: Tissue Engineering Opportunities forTissue engineering. Part B, Reviews · 2026Review
- Decellularized Extracellular Matrix Scaffolds to Engineer the Dormant Landscape of Microscopic Colorectal Cancer Liver Metastasis.Advanced healthcare materials · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Molecular and microenvironmental networks driving tumor dormancy: pathological mechanisms and emerging clinical strategies.Frontiers in medicine · 2026Review
- Expression profiling of inhibitory immune checkpoints in colorectal cancer stem cells and their association with tumor immunity and immunotherapy biomarkers.Frontiers in immunology · 2026Article
- Cancer Cell Dormancy and Chemotherapy Resistance.Journal of Cancer · 2026Review
- Exploration of the diagnostic and therapeutic potential of the nucleocytoplasmic shuttling protein TMUB1 by inducing G0/G1 cell cycle arrest in ovarian cancer.Molecular & cellular oncology · 2026Article
- Post-translational modification in hepatocellular carcinoma resistance: molecular mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
- Epigenetic regulation of NR5A2 influences colorectal cancer cell stemness via a stemness-related transcription factor NANOG.Cell communication and signaling : CCS · 2025Article
- Fatty acid binding protein 1 (FABP1) depletion promotes an oxidative metabolic shift in Caco-2 colorectal cancer cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2025Article
- Understanding Tumor Dormancy: from Experimental Models to Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2025Review
- Dormancy in Colorectal Carcinoma: Detection and Therapeutic Potential.Biomolecules · 2025Review
- The Nuclear Localization of ACLY Guards Early Embryo Development Through Recruiting P300 and HAT1 to Promote Histone Acetylation and Transcription.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cancer Stem Cells Connecting to Immunotherapy: Key Insights, Challenges, and Potential Treatment Opportunities.Cancers · 2025Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Dormant cancer cells drive recurrence and drug resistance, which lead to poor prognosis in colorectal cancer (CRC). The mechanisms that regulate the entry of cancer cells into dormancy remain to be extensively studied. Nanog is a master transcription factor to maintain the self-renewal and pluripotency of stem cells. Since dormant cancer cells are similar to quiescent cancer stem cells, the correlation between dormant state and Nanog in CRC is worth to be explored. Serum deprivation is a common method to establish experimental cellular dormancy model. Here, we verified that serum deprivation-induced CRC cells to enter a cellular dormancy state, characterized by no proliferation, no death, no senescence, resistance to chemotherapy, high expression of dormant markers, metabolic suppression, and recovery to active status. Interestingly, we further identified that Nanog was upregulated in dormant CRC cells. Nanog knockdown could destroy the dormant state of serum-deprived CRC cells while Nanog overexpression could induce dormancy in CRC cells. Mechanistically, Nanog was regulated through a fatty acid oxidation (FAO)/ATP citrate lyase (ACLY)-dependent pathway. FAO increased ACLY expression to promote the synthesis of acetyl-CoA, which was transferred by P300 to accelerate H3K27 acetylation of Nanog promoter. Then, Nanog upregulation increased the transcription of P21 and P27, which promoted the dormancy of CRC cells. Our findings revealed that Nanog could induce cellular dormancy in CRC cells and unlocked a specific mechanism to govern the process.
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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.