ArticleTranslational oncology2025
Exploration of the mechanism of 5-Methylcytosine promoting the progression of hepatocellular carcinoma.
Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- mBiology direct · 2026Review
- m5C-Related Regulators Define Tumor Microenvironment and Predict Prognosis in Hepatocellular Carcinoma.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Identification and validation of a prognostic signature of mJournal of thoracic disease · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
5-Methylcytosine (m5C) is a ubiquitous RNA modification that is closely related to various cellular functions. However, no studies have comprehensively demonstrated the role of m5C in hepatocellular carcinoma (HCC) progression. In this study, six pairs of HCC and adjacent tissue samples were subjected to methylated RNA immunoprecipitation sequencing to identify precise m5C loci. Non-negative matrix factorization (NMF) was used to identify HCC subtypes in TCGA-LIHC cohort. Immune, metabolic, and tumor-related pathways in HCC subtypes with differences in methylation status were analyzed and a prognostic model based on m5C-related genes was constructed. Finally, using RIP and molecular interaction analysis, we demonstrated that YBX1 binds to TPM3 in an m5C dependent manner and regulates HCC progression. Widespread m5C sites were identified and found to be differentially distributed in HCC compared with adjacent tissues. Metabolic processes were inhibited in hypermethylated HCC, whereas immune checkpoint and multiple classical tumor pathways were significantly upregulated. More importantly, we have identified an m5C dependent regulatory axis. The m5C reader YBX1 binds to TPM3 in an M5C dependent manner and promotes the progression of hepatocellular carcinoma. These results provide new evidence for further understanding the comprehensive role of m5C in HCC and the regulatory mechanism of m5C.
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.