ReviewJournal of translational medicine2023
Role of m6A modification in regulating the PI3K/AKT signaling pathway in cancer.
Review in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed.
- Interplay between N6-methyladenosine RNA methylation and protein lactylation: a novel crosstalk linking metabolism and epigenetic regulation in human diseases.Journal of translational medicine · 2026Review
- Abnormal Sialylation Promotes Chemotherapy Resistance in Bladder Cancer via the PI3K-AKT-mTOR Signaling Pathway.Cancers · 2026Article
- WTAP stabilized by USP7 contributes to enzalutamide resistance in prostate cancer via mediating AKT mCancer gene therapy · 2026Article
- Multi-omics and network pharmacology identify IGFBP1 as an m6A-Epigenetic target of pueraria in NSCLC therapy.PLoS computational biology · 2026Article
- Insulin signaling pathway related mNutrition & metabolism · 2026Article
- The Regulatory Role of mCells · 2026Review
- m6A modification and its clinical applications in gynaecological cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- HEG1 promotes gastric cancer progression by stabilizing AKT1 and is functionally regulated by the deubiquitinase USP48.European journal of medical research · 2025Article
- The Multifaceted Role of VIRMA, a Core Component of the Methyltransferase Complex, in Cancer and Cancer Therapy.Biomolecules · 2025Review
- FLOT1 Is a Novel Serum Biomarker of Ovarian Cancer Targeted by N6-methyladenosine Modification Inhibition.Cell biology international · 2025Article
- Reciprocal regulation between m6 A modifications and non-coding RNAs: emerging roles in cancer therapeutic resistance.Discover oncology · 2025Review
- Nitidine chloride inhibits the progression of hepatocellular carcinoma by suppressing IGF2BP3 and modulates metabolic pathways in an mMolecular medicine (Cambridge, Mass.) · 2025Article
- Emerging roles of non-coding RNAs in modulating the PI3K/Akt pathway in cancer.Non-coding RNA research · 2025Review
- Targeting the PI3K Pathway: Advancements and Achievements in Breast Cancer Therapy.Current pharmaceutical design · 2025Review
- Von Hippel Lindau tumor suppressor controls m6A-dependent gene expression in renal tumorigenesis.The Journal of clinical investigation · 2024Article
- Pathways and molecules for overcoming immunotolerance in metastatic gastrointestinal tumors.Frontiers in immunology · 2024Review
- The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphoinositide 3-kinase (PI3K)/AKT signaling pathway plays a crucial role in the pathogenesis of cancer. The dysregulation of this pathway has been linked to the development and initiation of various types of cancer. Recently, epigenetic modifications, particularly N6-methyladenosine (m6A), have been recognized as essential contributors to mRNA-related biological processes and translation. The abnormal expression of m6A modification enzymes has been associated with oncogenesis, tumor progression, and drug resistance. Here, we review the role of m6A modification in regulating the PI3K/AKT pathway in cancer and its implications in the development of novel strategies for cancer treatment.
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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.