ArticleClinical and experimental medicine2026
PSMC2 promotes hepatocellular carcinoma progression through interaction with EGFR.
Article in Clinical and experimental medicine, 2026. 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
Abstract
Growing evidence highlights the critical involvement of the ubiquitin-proteasome system in cancer development. As an essential component of the 26 S proteasome, Proteasome 26 S Subunit ATPase 2 (PSMC2) has been implicated in various malignancies, but its role in hepatocellular carcinoma (HCC) progression remains poorly understood. We analyzed PSMC2 expression using The Cancer Genome Atlas database (TCGA) database, and validated findings in clinical HCC specimens and cell lines through immunohistochemistry (IHC) and Western blot. Functional assays (CCK-8, colony formation, Scratch test and transwell invasion assay) were performed to assess the oncogenic properties of PSMC2 in the progression of HCC. Mechanistic studies employed co-immunoprecipitation, Western blot, immunofluorescence and in vivo xenograft models to investigate PSMC2-EGFR interactions and downstream signaling. PSMC2 was significantly overexpressed in HCC tissues and correlated with poor patient prognosis. Genetic knockdown of PSMC2 inhibited HCC cell proliferation, migration, and invasion in vitro, while suppressing tumor growth in vivo. Conversely, PSMC2 overexpression enhanced malignant phenotypes. Mechanistically, PSMC2 physically interacted with EGFR, stabilizing EGFR protein levels and enhancing phosphorylation of downstream AKT and ERK1/2 pathways. Our study identifies PSMC2 as a novel regulator of HCC progression through EGFR-AKT/ERK1/2 signaling axis activation. These findings position PSMC2 as both a prognostic biomarker and a potential therapeutic target for HCC intervention.
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.