ReviewCell proliferation2022
Insights into roles of METTL14 in tumors.
Review in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 45 citations in OpenAlex.
- Regulatory roles of N6-methyladenosine methylation factors in melanoma invasion and metastasis (Review).Oncology letters · 2026Review
- RBM15 in diseases: Molecular mechanisms and clinical opportunities from RNA mGenes & diseases · 2026Review
- RNA epitranscriptomic regulation of tumor immune evasion: mechanisms, context-dependent roles, and therapeutic implications.Frontiers in immunology · 2026Review
- Mechanism of METTL14-mediated RAD21 mRNA epigenetic transcriptome modification in inhibiting thyroid cancer development.World journal of surgical oncology · 2025Article
- METTL3 and METTL14 drive pancreatic adenocarcinoma progression via m6A-dependent alternative splicing in PANC-1 cells.Discover oncology · 2025Article
- Role of m6A RNA methylation regulators in pancreatic cancer: interactions and potential implications.Cancer cell international · 2025Review
- METTL14 induces ferroptosis to inhibit colorectal cancer progression by inhibiting TRIB3 via an m6A-YTHDF2-dependent manner.Journal of molecular histology · 2025Article
- Pan-cancer oncogenic properties and therapeutic potential of SF3B4.Cancer gene therapy · 2025Article
- m6A methylation: a new frontier in epilepsy research and therapeutics.EXCLI journal · 2025Review
- New insights into N6-methyladenosine in hepatocellular carcinoma immunotherapy.Frontiers in immunology · 2025Review
- Exosomal long non-coding RNA-LINC00839 promotes lung adenocarcinoma progression by activating NF-κB signaling pathway.Annals of medicine · 2024Article
- Crosstalk Between m6A RNA Methylation and miRNA Biogenesis in Cancer: An Unholy Nexus.Molecular biotechnology · 2024Review
- Regulation of mFunctional & integrative genomics · 2024Review
- Pan-cancer Analysis Reveals m6A Variation and Cell-specific Regulatory Network in Different Cancer Types.Genomics, proteomics & bioinformatics · 2024Article
- METTL14 Suppresses Tumor Stemness and Metastasis of Colon Cancer Cells by Modulating m6A-Modified SCD1.Molecular biotechnology · 2024Article
- N6-methyladenosine modification of hypoxia-inducible factor-1α regulatesWorld journal of gastrointestinal oncology · 2024Article
- WTAP-induced NCancer science · 2024Article
- Emerging role of RNA modification and long noncoding RNA interaction in cancer.Cancer gene therapy · 2024Review
- METTL14/miR-29c-3p axis drives aerobic glycolysis to promote triple-negative breast cancer progression though TRIM9-mediated PKM2 ubiquitination.Journal of cellular and molecular medicine · 2024Article
- Targeting key RNA methylation enzymes to improve the outcome of colorectal cancer chemotherapy (Review).International journal of oncology · 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 at 1 institution in 1 country.
Funding
Abstract
N6-Methyladenosine (m6A) is considered the most common and endogenous modification of eukaryotic RNAs. Highly conserved in many species, m6A regulates RNA metabolism, cell differentiation, cell circadian rhythm, and cell cycle; it also responds to endogenous and exogenous stimuli and is associated with the development of tumors. The m6A methyltransferase complex (MTC) regulates the m6A modification of transcripts and involves two components, methyltransferase-like enzyme 3 (METTL3) and methyltransferase-like enzyme 14 (METTL14), and other auxiliary regulatory distinct components. Though with no catalytic effect, METTL14 serves as an RNA-binding scaffold in MTC, promotes RNA substrate recognition, activates, and escalates the catalytic capability of METTL3, thus accounting for a pivotal member of the complex. It was reported that METTL14 regulates tumor proliferation, metastasis, and self-renewal, and plays a part in tumorigenesis, tumor progression, and other processes. The present work is a review of the role of METTL14 both as a tumor suppressor and a tumor promoter in the oncogenesis and progression of various tumors, as well as the potential molecular mechanisms.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.