ArticleInternational journal of oncology2022
METTL3 antagonizes 5‑FU chemotherapy and confers drug resistance in colorectal carcinoma.
Article in International journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting m6A-SCG2-TAMs axis overcomes 5-FU resistance in colorectal cancer via a multi-omics model.NPJ digital medicine · 2026Article
- METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review).International journal of oncology · 2026Review
- TBKBP1 induces capecitabine resistance through negative regulation of type I interferon pathway in triple-negative breast cancer.Oncogene · 2026Article
- Preparation and Antitumor Activity of METTL3 SiRNA Nanoparticles Carried by Hypoxia Sensitive Polymer (mPEG-Azo-PEI).International journal of nanomedicine · 2026Article
- METTL3 in colorectal cancer: molecular insights and clinical implications.Molecular biology reports · 2025Review
- The bidirectional regulatory effects of bacteria on blood vessels in the tumor microenvironment.Discover oncology · 2025Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Dissecting the METTL3/STC2 axis in colorectal cancer: implications for drug resistance and metastasis.Cell biology and toxicology · 2025Article
- Switching from messenger RNAs to noncoding RNAs,World journal of gastrointestinal oncology · 2025Review
- Article
- NEK2 promotes cancer cell progression and 5-fluorouracil resistance via the Wnt/β-catenin signaling pathway in colorectal cancer.Discover oncology · 2025Article
- Huaier promotes sensitivity of colorectal cancer to oxaliplatin by inhibiting METTL3 to regulate the Wnt/β‑catenin signaling pathway.Oncology reports · 2025Article
- Mitochondrial Deoxyguanosine Kinase Induces 5-Fluorouracil Chemotherapy Sensitivity through Autophagy.Current cancer drug targets · 2025Article
- Targeting key RNA methylation enzymes to improve the outcome of colorectal cancer chemotherapy (Review).International journal of oncology · 2024Review
- BRD7 enhances the radiosensitivity of nasopharyngeal carcinoma cells by negatively regulating USP5/METTL3 axis-mediated homologous recombination repair.International journal of biological sciences · 2024Article
- METTL3-mediated mEpigenetics · 2023Article
- New insights into the regulation of METTL3 and its role in tumors.Cell communication and signaling : CCS · 2023Review
- Colitis-associated carcinogenesis: crosstalk between tumors, immune cells and gut microbiota.Cell & bioscience · 2023Review
- [Research Advances of RAD51AP1 in Tumor Progression and Drug Resistance].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Review
- Methyltransferase-like proteins in cancer biology and potential therapeutic targeting.Journal of hematology & oncology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is one of top five leading causes of cancer‑associated mortalities worldwide. 5‑Fluorouracil (5‑FU) is the first‑line chemotherapeutic drug in the treatment of CRC; however, its antineoplastic efficiency is limited due to acquired drug resistance. The regulatory mechanism underlying 5‑FU chemotherapeutic response and drug resistance in CRC remains largely unknown. The present study identified that silencing of methyltransferase‑like 3 (METTL3) suppressed the proliferation and migration of CRC HCT‑8 cells. Using cell survival assays, flow cytometric and colony formation analyses, it was revealed that inhibition of METTL3 sensitized HCT‑8 cells to 5‑FU by enhancing DNA damage and inducing apoptosis in HCT‑8 cells under 5‑FU treatment. Furthermore, the expression of METTL3 was upregulated in 5‑FU‑resistant CRC cells (HCT‑8R), which contributed to drug resistance through regulation of RAD51 associated Protein 1 (RAD51AP1) expression. Western blotting, immunofluorescence staining and drug sensitivity assays demonstrated that knockdown of METTL3 augmented 5‑FU‑induced DNA damage and overcame 5‑FU‑resistance in HCT‑8R cells, which could be mimicked by inhibition of RAD51AP1. The present study revealed that the METTL3/RAD51AP1 axis plays an important role in the acquisition of 5‑FU resistance in CRC, and targeting METTL3/RAD51AP1 may be a promising adjuvant therapeutic strategy for patients with CRC, particularly for those with 5‑FU‑resistant CRC.
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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.