ArticleRedox biology2022
CPT1A promotes anoikis resistance in esophageal squamous cell carcinoma via redox homeostasis.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 63 citations in OpenAlex.
- Efficacy and safety of TAS-102 plus Surufatinib in third and later line metastatic pancreatic cancer: a prospective, single center and biomarker exploratory, phase II study.Molecular cancer · 2025Trial
- ASB3 degrades the gateway to β-oxidation: Editorial on "Hepatocytic ankyrin repeat and SOCS box protein 3 deficiency alleviates metabolic dysfunction-associated steatotic liver disease by decreasing ubiquitin-mediated carnitine palmitoyl transferase 1A".Clinical and molecular hepatology · 2026Article
- HOXC9 accelerates esophageal squamous cell carcinoma progression via OTUD1-FABP5-mediated lipid metabolic reprogramming.Cell death & disease · 2026Article
- TRIM32-mediated ABI2 downregulation promotes anoikis resistance and metastasis by regulating EMT in lung adenocarcinoma.Cellular and molecular life sciences : CMLS · 2026Article
- Nanoparticle-based strategies targeting disulfidptosis, anoikis, and PANoptosis for enhanced cancer therapy.Journal of nanobiotechnology · 2026Review
- MMP7-Triggered mitophagy by regulating parkin-mediated ubiquitination of VDAC1 confers anoikis resistance in the epithelium of hyperplastic prostate.Cell death & disease · 2026Article
- CPT1A drives cisplatin resistance via acetylation‑dependent activation of DRP1 and mitochondrial fission in small cell lung cancer.Cell death & disease · 2026Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Detachment-Induced FAK-STAT3-NNMT Inhibits CTCs Anoikis to Promote Breast Cancer Metastasis by Enhancing Fatty Acid Oxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Regulatory Potential of piRNAs TargetingGenes · 2026Article
- Liquiritin restores metabolic homeostasis in NAFLD by modulating AKT1/FOXO1 signaling.Frontiers in pharmacology · 2026Article
- The emerging metabolic role and treatment target of CPT1A in CRC.Frontiers in cell and developmental biology · 2026Review
- NR4A3 regulates anoikis resistance and metastasis of bladder cancer through EWSR1.Cancer biology & therapy · 2025Article
- CPT1A facilitated ferroptosis by forming feedback loop with Nrf2 via PI3K/AKT pathway in colorectal cancer.Apoptosis : an international journal on programmed cell death · 2025Article
- Novel therapeutic strategies for targeting fatty acid oxidation in cancer.Biomarker research · 2025Review
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- Exploring the Role of LINC00115 in Esophageal Squamous Cell Carcinoma: Insights Into JAK1/STAT3 Pathway Activation and Metastatic Potential.JCO precision oncology · 2025Article
- Construction and validation of an anoikis-related long non-coding RNA-based prognostic model for head and neck squamous cell carcinoma.Translational cancer research · 2025Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anoikis resistance was a prominent hallmark of cancer metastasis, and lipo-genic characteristics have been identified as another metabolic alteration during tumorigenesis. However, their crosstalk has not been fully elucidated, especially in advanced esophageal squamous cell carcinoma (ESCC). In this study, we showed, for the first time, that the key enzyme carnitine O-palmitoyl transferase 1 (CPT1A), which is involved in fatty acid oxidation (FAO), was markedly upregulated in ESCC cells upon detached culture via a metabolism PCR array. Overexpression of CPT1A was associated with poor survival of ESCC patients and could protect ESCC cells from apoptosis via maintaining redox homeostasis through supply of GSH and NADPH. Mechanistically, detached culture conditions enhanced the expression of the transcription factor ETV4 and suppressed the expression of the ubiquitin enzyme RNF2, which were responsible for the elevated expression of CPT1A at the mRNA and protein levels, respectively. Moreover, genetic or pharmacologic disruption of CPT1A switched off the NADPH supply and therefore prevented the anchorage-independent growth of ESCC cells in vitro and lung metastases of xenografted tumor models in vivo. Collectively, our results provide novel insights into how ESCC cancer cells exploit metabolic switching to form distant metastases and some evidence for the link between anoikis and FAO.
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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.