ArticleAging2023
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Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 38 citations in OpenAlex.
- METTL16 promotes colorectal cancer progression and CD8Medical oncology (Northwood, London, England) · 2026Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- IL-23 promotes PD-L1 expression and tumor immune evasion via METTL16 pathway.American journal of cancer research · 2026Article
- Adenosine signaling in tumor immune escape: metabolic checkpoints, myeloid suppression, and combination immunotherapy.Frontiers in oncology · 2026Review
- Regulation and application of mScience China. Life sciences · 2025Review
- METTL16 emerges as a pivotal epitranscriptomic regulator, linking RNA modification, tumor progression, and immune modulation.Frontiers in immunology · 2025Review
- RNA modifications in cancer.MedComm · 2025Review
- Regulation of RNA methylation linked to drug resistance in gastric cancer.Frontiers in cell and developmental biology · 2025Review
- METTL16 Promotes Lipid Metabolic Reprogramming and Colorectal Cancer Progression.International journal of biological sciences · 2025Article
- Modulation of host N6-methyladenosine modification by gut microbiota in colorectal cancer.World journal of gastroenterology · 2024Review
- METTL protein family: focusing on the occurrence, progression and treatment of cancer.Biomarker research · 2024Review
- Multifaceted bioinformatic analysis of m6A-related ferroptosis and its link with gene signatures and tumour-infiltrating immune cells in gliomas.Journal of cellular and molecular medicine · 2024Article
- Role of N6-methyladenosine RNA modification in cancer.MedComm · 2024Review
- METTL Family in Healthy and Disease.Molecular biomedicine · 2024Review
- The role of RNA methylation in tumor immunity and its potential in immunotherapy.Molecular cancer · 2024Review
- ALKBH5 promotes non-small cell lung cancer progression and susceptibility to anti-PD-L1 therapy by modulating interactions between tumor and macrophages.Journal of experimental & clinical cancer research : CR · 2024Article
- RNA modifications in cancer immune therapy: regulators of immune cells and immune checkpoints.Frontiers in immunology · 2024Review
- Bibliometric analysis and visualization of the research on the relationship between RNA methylation and immune cell infiltration in tumors.Frontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe immune checkpoint inhibitors (ICIs) has dramatically changed the therapeutic area of cancers. A great number of patients with CRC exhibit poor response rate to ICI treatment. N6-methyl adenosine (m6A) is closely correlated with the initiation and progression of cancers. To explore the role of methyltransferase-like 16 (METTL16) in CRC treatment.
methodsClinical samples and different CRC cell lines were collected. The expression of METTL16 and PD-L1 was determined by qPCR, IHC. Ectopic expression of METTL16 was performed in CRC cells. A co-culture system was established using CRC cells and T cells to measure the immune evasion. Cell viability, apoptosis, migration, and invasion were examined by CCK-8, colony formation, flow cytometry, Transwell, and wound healing assay, respectively. The N6-methyl adenosine (m6A) modification of PD-L1 by METTL16 was investigated by methylated RIP (MeRIP) and RNA stability experiment.
resultsMETTL16 was decreased and PD-L1 was increased in CRC tissues and cell lines. METTL16 enhanced cell proliferation, migration, and invasion, and promoted CRC tumor growth
conclusionsOur work identified the METTL16/PD-L1/PD-1 regulatory axis in CRC development and immune evasion, which represented a promising target for CRC treatment.
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.