ArticleCell division2025
Mitochondrial fission regulator 2 promotes cell proliferation, migration and invasion in hepatocellular carcinoma through regulating PI3K/AKT signaling pathway.
Article in Cell division, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- MTFR2 regulated the proliferation, apoptosis, migration, and invasion of endometrial cancer cells through the Drp1/MFN1 signaling pathway mediated mitochondrial fission.Translational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMitochondrial fission regulator 2 (MTFR2) is upregulated in multiple cancers, including hepatocellular carcinoma (HCC); however, its mechanistic role in HCC progression remains poorly understood.
methodsMTFR2 expression in HCC tissues was analyzed using TCGA and GEO databases. Validation of MTFR2 expression levels in clinical samples and HCC cell lines was performed through qRT-PCR and western blot. Functional effects of MTFR2 overexpression and knockdown on HCC cell proliferation, migration, and invasion were assessed via CCK-8, colony formation, wound healing, and transwell assays. In vivo tumor growth was evaluated in xenograft mouse models.
resultsMTFR2 was significantly overexpressed in HCC tissues and cell lines. Enhanced proliferation, migration, invasion, and colony formation were observed in MTFR2-overexpressing HCC cells, whereas knockdown of MTFR2 suppressed these malignant phenotypes. Mechanistic studies demonstrated that MTFR2 promotes proliferation, migration, and invasion of HCC cells via the PI3K/AKT signaling pathway. Additionally, MTFR2 knockdown significantly attenuated tumor growth in xenograft models.
conclusionThese findings demonstrate that MTFR2 promotes HCC progression via modulation of the PI3K/AKT pathway, underscoring its potential as a therapeutic target for HCC.
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.