ArticleFrontiers in immunology2025
CHMP4A in hepatocellular carcinoma: exploring its role in tumor progression, immune modulation, and potential link to TIM3 checkpoint.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Background: Charged Multivesicular Body Protein 4A (CHMP4A), a member of the ESCRT-III family, plays a pivotal role in membrane remodeling and fission, with emerging evidence underscoring its significance in cancer immunotherapy. The complex pathogenesis and therapeutic resistance characteristic of liver hepatocellular carcinoma (LIHC) present significant challenges in clinical practice. This study investigated the potential involvement of CHMP4A in the progression of LIHC. Methods and results: Utilizing a comprehensive pan-cancer analysis with datasets from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), ArrayExpress database and the International Cancer Genome Consortium (ICGC), we evaluated the prognostic significance of CHMP4A, its clinical implications, associated signaling pathways, DNA methylation status, immune cell infiltration, and response to chemotherapy. Bioinformatics analyses, corroborated by immunohistochemical validation, revealed a marked overexpression of CHMP4A in LIHC specimens relative to adjacent normal tissues. Kaplan-Meier survival analyses indicated that this elevated expression pattern was associated with poor patient outcomes. Single-cell transcriptomic analysis had identified NK/T cells and tumor cells as the predominant cellular sources of CHMP4A within the LIHC microenvironment. Functional studies employing CHMP4A-specific small interfering RNA (siRNA) revealed significant inhibition of malignant phenotypes in LIHC cells, notably affecting proliferation, migration, and invasive capabilities. Mechanistically, the knockdown of CHMP4A led to modulation of the epithelial-mesenchymal transition (EMT), as indicated by the upregulation of E-cadherin and the concurrent downregulation of vimentin and matrix metalloproteinases (MMP-2/9). A comprehensive analysis of the immune landscape demonstrated significant correlations between CHMP4A expression patterns and various immunological parameters, including immune cell infiltration, expression of checkpoint molecules, tumor mutational burden (TMB), and microsatellite instability (MSI). Notably, the silencing of CHMP4A markedly decreased the expression levels of the TIM3/LGALS9 immune checkpoint axis in LIHC. Conclusions: Our extensive analyses identified CHMP4A as a critical molecular determinant in the progression of LIHC, which may function through two oncogenic mechanisms: the promotion of tumor cell proliferation and metastatic potential, and immunomodulatory effects associated with the TIM3/LGALS9 signaling pathway. These findings indicated that CHMP4A might serve as a potential therapeutic target and prognostic biomarker in LIHC.
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.