ReviewMedComm2024
Role of N6-methyladenosine RNA modification in cancer.
Review in MedComm, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed.
- ZC3H13-mediated m6A stabilization of CCND1 promotes malignant progression and is associated with poor anti-PD-1 response in HNSCC.Clinical and translational medicine · 2026Article
- A m6A/m1A/m5C-related eight-gene signature predicts prognosis and correlates with immune microenvironment in pediatric acute myeloid leukemia.Translational pediatrics · 2026Article
- An m6A-programmed cell death signature predicts prognosis and identifies STK25 as a therapeutic target in colon adenocarcinoma.Oncology letters · 2026Article
- The Role of NMedComm · 2026Review
- Abnormal Sialylation Promotes Chemotherapy Resistance in Bladder Cancer via the PI3K-AKT-mTOR Signaling Pathway.Cancers · 2026Article
- m6A modification-mediated lncRNA UNC5B-AS1 enhances HCC progression through miR-760/IL6 axis.Scientific reports · 2026Article
- The m6A reader IGF2BP3 promotes triple-negative breast cancer metastasis through HOXB9-IL15RA pathway.Functional & integrative genomics · 2026Article
- MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Exosomal bioactive molecules: molecular regulation, functional heterogeneity, and translational implications in disease diagnostics and therapeutics.Clinical and experimental medicine · 2026Review
- NAT10 and ac4C modification in cancer immunity and metabolism: emerging mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- The mechanistic role of Wilms tumor 1-associated protein in cancer pathogenesis, immunity, immunotherapy, and therapy resistance.Investigational new drugs · 2026Review
- ALKBH5 promotes gastric cancer angiogenesis by stabilizing LncRNA PVT1 and VEGFA RNAs via m6A demethylation.Molecular and cellular biochemistry · 2026Article
- Article
- N4-acetylcytidine modification bridges metabolic reprogramming and immune evasion in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Mechanism and therapeutic prospects of ferroptosis regulation through m6A in cancer.Frontiers in cell and developmental biology · 2026Review
- NScientific reports · 2025Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- MondoA mediates transcriptional coordination between the MYC network and the integrated stress response in pancreatic ductal adenocarcinoma.bioRxiv : the preprint server for biology · 2025Article
- Enhancing doxorubicin sensitivity in osteosarcoma via iRGD-modified biomimetic nanoparticles targeting MCAM m6A modification.Journal of translational medicine · 2025Article
- The Malignant Transformation of Viral Hepatitis to Hepatocellular Carcinoma: Mechanisms and Interventions.MedComm · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N6-methyladenosine (m6A) is the most abundant modification of RNA in eukaryotic cells. Previous studies have shown that m6A is pivotal in diverse diseases especially cancer. m6A corelates with the initiation, progression, resistance, invasion, and metastasis of cancer. However, despite these insights, a comprehensive understanding of its specific roles and mechanisms within the complex landscape of cancer is still elusive. This review begins by outlining the key regulatory proteins of m6A modification and their posttranslational modifications (PTMs), as well as the role in chromatin accessibility and transcriptional activity within cancer cells. Additionally, it highlights that m6A modifications impact cancer progression by modulating programmed cell death mechanisms and affecting the tumor microenvironment through various cancer-associated immune cells. Furthermore, the review discusses how microorganisms can induce enduring epigenetic changes and oncogenic effect in microorganism-associated cancers by altering m6A modifications. Last, it delves into the role of m6A modification in cancer immunotherapy, encompassing RNA therapy, immune checkpoint blockade, cytokine therapy, adoptive cell transfer therapy, and direct targeting of m6A regulators. Overall, this review clarifies the multifaceted role of m6A modification in cancer and explores targeted therapies aimed at manipulating m6A modification, aiming to advance cancer research and improve patient outcomes.
Indexed as
Identifiers
What Socratic holds
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.