ReviewHeliyon2023
N6-methyladenosine (m6A) as a regulator of carcinogenesis and drug resistance by targeting epithelial-mesenchymal transition and cancer stem cells.
Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
13 citing papers in PubMed, 19 citations in OpenAlex.
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- YTHDF3 Promoted Gastric Cancer Progression by Facilitating mAnalytical cellular pathology (Amsterdam) · 2026Article
- ALKBH5-mediated NPC2 mRNA mFunctional & integrative genomics · 2025Article
- Emerging Concepts in Immuno-Oncology: Insights from Natural Language Processing-Driven Co-Occurrence Analysis.ACS omega · 2025Review
- CD133-Guided RNA Nanoparticle Delivery of FTO siRNA Impairs Leukemia Resistance to Tyrosine Kinase Inhibitor Therapy.RNA nanomed · 2025Article
- Molecular mechanism of ZC3H13 -mediated ferroptosis in doxorubicin resistance of triple negative breast cancer.Cell biology and toxicology · 2025Article
- Epigenetic regulation of reprogramming and pluripotency: insights from histone modifications and their implications for cancer stem cell therapies.Frontiers in cell and developmental biology · 2025Review
- Research progress on m6A and drug resistance in gastrointestinal tumors.Frontiers in pharmacology · 2025Review
- Influence of RNA Methylation on Cancerous Cells: A Prospective Approach for Alteration of In Vivo Cellular Composition.Advances in experimental medicine and biology · 2025Review
- Role of N6-methyladenosine methylation in nasopharyngeal carcinoma: current insights and future prospective.Cell death discovery · 2024Review
- Interplay of RNA mBiomedicines · 2024Article
- Decoding the molecular symphony: interactions between the mNAR cancer · 2024Review
- Examining the evidence for mutual modulation between m6A modification and circular RNAs: current knowledge and future prospects.Journal of experimental & clinical cancer research : CR · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emergence of drug resistance to chemotherapeutic agents is the principal obstacle towards curative cancer treatment in human cancer patients. It is in an urgent to explore the underlying molecular mechanisms to overcome the drug resistance. N6-Methyladenosine (m6A) RNA modification is the most abundant reversible RNA modification and has emerged in recent years to regulate gene expression in eukaryotes. Recent evidence has identified m6A is associated with cancer pathogenesis and drug resistance, contributing to the self-renewal and differentiation of cancer stem cell, tumor epithelial-mesenchymal transition (EMT) and tumor metastasis. Here we reviewed up-to-date knowledge of the relationship between m6A modulation and drug resistance. Furthermore, we illustrated the underlying mechanisms of m6A modulation in drug resistance. Lastly, we discussed the regulation of m6A modulation in EMT and cancer stem cells. Hence, it will help to provide significant therapeutic strategies to overcome drug resistance for cancer patients by changing m6A-related proteins via targeting cancer stem cells and EMT-phenotypic cells.
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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 Socratic graph.