ArticleAging2019
Overexpressed methyltransferase-like 1 (METTL1) increased chemosensitivity of colon cancer cells to cisplatin by regulating miR-149-3p/S100A4/p53 axis.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
78 citing papers in PubMed, 144 citations in OpenAlex.
- METTL1/WDR4 Complex: A Novel Epitranscriptomic Target at the Crossroads of RNA Methylation and Drug Discovery.Journal of medicinal chemistry · 2026Review
- Article
- N7-Methylguanosine Modification in Colorectal Cancer: Molecular Insights and Clinical Implications.International journal of molecular sciences · 2026Review
- METTL1-Mediated MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RNA modification systems as therapeutic targets.Nature reviews. Drug discovery · 2026Review
- The methyltransferase-like proteins as core regulators of nucleic acid modifications and post-translation modification of proteins in disease pathogenesis and therapeutic implications.Biomarker research · 2025Review
- m7G RNA methylation in cancer: Effect, mechanism and clinical application.Clinical and translational medicine · 2025Review
- Role of S100 family proteins in colorectal cancer (CRC): an overview of their potential function as new biomarkers and therapeutic agents.Expert reviews in molecular medicine · 2025Review
- Identification of hub genes predicting sensitivity to neoadjuvant chemoradiation in locally advanced rectal cancer.Radiology and oncology · 2025Article
- Integrative bioinformatics analysis identifies METTL1 as a regulator of immune infiltration and prognosis in breast cancer.Scientific reports · 2025Article
- Targeting epigenetic regulators as a promising avenue to overcome cancer therapy resistance.Signal transduction and targeted therapy · 2025Review
- RNA epigenetic modifications as dynamic biomarkers in cancer: from mechanisms to clinical translation.Biomarker research · 2025Review
- Modifications of RNA in cancer: a comprehensive review.Molecular biology reports · 2025Review
- The diverse landscape of RNA modifications in cancer development and progression.Genes & genomics · 2025Review
- Deciphering the secret codes in NClinical and translational medicine · 2025Review
- Combating Methotrexate Resistance in Cancer Treatment: A Review on Navigating Pathways and Enhancing Its Efficacy With Fat-Soluble Vitamins.Scientifica · 2025Review
- METTL1 in human cancers: recognition of their functions, mechanisms and therapeutic value.Oncology reviews · 2025Review
- miR-149-3p targetingBiomolecules & biomedicine · 2024Article
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Writers, readers, and erasers RNA modifications and drug resistance in cancer.Molecular cancer · 2024Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methyltransferase-like 1 (METTL1) mediated 7-methylguanosine (m7G) is crucial for the regulation of chemoresistance in cancer treatment. However, the role of METTL1 in regulating chemoresistance of colon cancer (CC) cells to cisplatin is still unclear. This study established the cisplatin-resistant CC (CR-CC) cells and found that METTL1 was low-expressed in CR-CC cells compared to their paired cisplatin-sensitive CC (CS-CC) cells. Besides, overexpressed METTL1 enhanced the cytotoxic effects of cisplatin on CR-CC cells. In addition, miR-149-3p was the downstream target of METTL1, which could be positively regulated by METTL1. Further results validated that miR-149-3p was low-expressed in CR-CC cells comparing to the CS-CC cells. In addition, the promoting effects of overexpressed METTL1 on cisplatin induced CR-CC cell death were abrogated by synergistically knocking down miR-149-3p. Furthermore, S100A4/p53 axis was the downstream target of METTL1 and miR-149-3p, and either overexpressed METTL1 or miR-149-3p increased p53 protein levels in CR-CC cells, which were reversed by upregulating S100A4. Similarly, the promoting effects of overexpressed METTL1 on cisplatin-induced CR-CC cell death were abrogated by overexpressing S100A4. Taken together, overexpression of METTL1 sensitized CR-CC cells to cisplatin by modulating miR-149-3p/S100A4/p53 axis.
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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.