ArticleBiology direct2024
CircHIF1A induces cetuximab resistance in colorectal cancer by promoting HIF1α-mediated glycometabolism alteration.
Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Glucose Transporter 1 in Health and Disease.MedComm · 2026Review
- Lactate metabolic reprogramming and lactylation modification: molecular mechanisms reshaping the tumor immunosuppressive microenvironment.Cell & bioscience · 2026Review
- CircRNA circuits orchestrate lactate metabolism in gastrointestinal cancer progression.Open life sciences · 2026Article
- Non-Coding RNAs and cernas: emerging modulators of drug response in colorectal cancer.Molecular biology reports · 2025Review
- Review
- Extracellular vesicles circular RNA: A new perspective and clinical application potential for mediating chemoresistance in colorectal cancer.World journal of clinical oncology · 2025Review
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- Epacadostat Overcomes Cetuximab Resistance in Colorectal Cancer by Targeting IDO-Mediated Tryptophan Metabolism.Cancer science · 2025Article
- Targeting ncRNAs to overcome metabolic reprogramming‑mediated drug resistance in cancer (Review).International journal of oncology · 2025Review
- Warburg effect and lactylation in cancer: mechanisms for chemoresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- Unveiling Pharmacogenomics Insights into Circular RNAs: Toward Precision Medicine in Cancer Therapy.Biomolecules · 2025Review
- Role of circular RNAs in cancer therapy resistance.Molecular cancer · 2025Review
- Exploring the Link Between Noncoding RNAs and Glycolysis in Colorectal Cancer.Journal of cellular and molecular medicine · 2025Review
- A Machine Learning-Based Hypoxia-Related Gene Signatures to Facilitate Prediction of Cetuximab Response in Patients with Colorectal Cancer.International journal of medical sciences · 2025Article
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
- CircRNAs in colorectal cancer: potential roles, clinical applications, and natural product-based regulation.Frontiers in oncology · 2025Review
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
- Lactylation in cancer: Mechanisms in tumour biology and therapeutic potentials.Clinical and translational medicine · 2024Review
- Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR)-targeted therapy is an important treatment for RAS wild-type metastatic colorectal cancer (mCRC), but the resistance mechanism remains unclear. Here, the differential expression of circRNAs between Cetuximab sensitive and resistant cell lines was analyzed using whole-transcriptome sequencing. We identified that the expression of circHIF1A was significantly higher in LIM1215-R than in LIM1215. When treated with Cetuximab, downregulation of circHIF1A level weakened the proliferation and clonal formation ability of LIM1215-R, caused more cells to enter G0-G1 phase, and significantly reduced the basal respiration, ATP production, and maximal respiration, as well as the glycolytic capacity and glycolytic reserve. The response rate and prognosis of circHIF1A-positive patients were inferior to those of negative patients. Mechanistically, circHIF1A can upregulate the level of hypoxia-inducible factor 1 A (HIF1A) by competitively binding to miR-361-5p, inducing the overexpression of enzymes such as glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA). In a xenograft model, inhibition of circHIF1A expression increased the sensitivity to Cetuximab treatment. In conclusion, circHIF1A can promote HIF1α-mediated glycometabolism alteration to induce Cetuximab resistance in CRC. It has the potential to become a screening indicator for the Cetuximab beneficial population in mCRC and a new therapeutic target for enhancing treatment efficacy.
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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.