ArticleCellular oncology (Dordrecht, Netherlands)2023
In vivo study revealed pro-tumorigenic effect of CMTM3 in hepatocellular carcinoma involving the regulation of peroxisome proliferator-activated receptor gamma (PPARγ).
Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 11 citations in OpenAlex.
- MiR-218-5p inhibits glioma progression by targeting CKLF-like MARVEL transmembrane domain-containing 3.BMC cancer · 2026Article
- The Bioinformatics Analysis of Publicly Available Datasets and Validation in a Mouse Model of Myocardial Infarction Through Coronary Artery Ligation.Journal of inflammation research · 2026Article
- CMTM3 promotes adipocyte differentiation by regulating PPARγ in 3T3-L1 cells.Genes & diseases · 2025Article
- Polyphyllin I exerts anti-hepatocellular carcinoma activity by targeting ZBTB16 to activate the PPARγ/RXRα signaling pathway.Chinese medicine · 2024Article
- Review
- Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo clarify the ambiguity of the function of CMTM3 in the development of hepatocellular carcinoma (HCC) and explore its molecular mechanism.
methodsThe Cmtm3-KO C57BL/6 mouse strain was established using CRISPR-Cas9. Acute liver damage and HCC models were induced by peritoneal injection of 100 or 25 mg/kg.BW N-Nitrosodiethylamine (DEN) to male mice. Liver function and histology were evaluated by blood serum levels of AST and ALT, and HE staining. Gene and protein expression in liver tissues was investigated by RNA-seq, RT-qPCR, Western blotting, immunohistochemistry, and immunofluorescence. Protein-protein interactions were studied by STRING and topological measures. The mRNA expression of CMTM3 and PPARs and patient survival were analyzed using the UALCAN database.
resultsGlobal knockout of Cmtm3 in KO mice was successfully confirmed. Cmtm3 knockout alleviated DEN-induced acute damage to liver histological integrity and liver function, reduced DNA damage and apoptosis, and also caused a significantly reduced number (WT: 8.7 ± 5.5 vs. KO: 2.7 ± 3.1, P = 0.0394) and total size of tumors (WT: 130.9 ± 181.8 mm
conclusionThis study clarified the pro-tumorigenesis role of CMTM3 in HCC in vivo, possibly through the upregulation of PPARγ and activation of the PPAR pathway.
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.