ArticleJournal of oncology2022
Methyltransferase-like 3 Aggravates HCC Development via Mediating N6-Methyladenosine of Ubiquitin-Specific Protease 7.
Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 2 citations in OpenAlex.
- It takes two to tango: the intersection of deubiquitinases and mMolecular cancer · 2026Review
- Roles of RNA Methylations in Cancer Progression, Autophagy, and Anticancer Drug Resistance.International journal of molecular sciences · 2023Review
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
We aimed to investigate the role of methyltransferase-like 3 (METTL3) in regulating HCC by mediating m6A level of ubiquitin-specific protease (USP7). METTL3 levels and m6A contents in HCC tissues and cells were detected. Potential correlations between METTL3 level and lymphatic metastasis, tumor size, tumor staging, and overall survival of HCC patients were analyzed. Moreover, its regulatory effects on proliferative, migratory, and invasive rates of HCC cells were examined. Potential methylation of USP7 in HCC was predicted using an online software, and the correlation between USP7 and METTL3 was assessed. METTL3 and m6A were increased both in HCC cells and tissues. High level of METTL3 was associated with the incidence of lymphatic metastasis, large tumor size, advanced tumor staging, and low overall survival of HCC. Silencing of METTL3 reduced proliferation, migration, and invasion rates. USP7 was predicted to have a methylation site regulated by METTL3. It was upregulated in HCC and associated with METTL3 level positively. USP7 silencing decreased proliferation, migration, and invasion rates of HCC cells. METTL3 promotes HCC to proliferate, migrate, and invade by regulating m6A methylation of USP7.
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.