ArticleScientific reports2025
Pan-cancer analysis of oncogenic role of MAGOH and experiment validation in hepatocellular carcinoma.
Article in Scientific reports, 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
9 authors.
Funding
Abstract
Several studies have highlighted that Mago-nashi homolog (MAGOH) contributed greatly to cell development, growth, and malignant progression in multiple cancer types. Nevertheless, the role of MAGOH in pan-cancer datasets, particularly in hepatocellular carcinoma (HCC), remains uninvestigated. In this study, we first utilized diverse databases to systematically analyze the expression and significance of MAGOH across pan-cancer. Besides, we validated the clinical significance and biological functions of MAGOH in HCC via clinical specimens and in vitro experiments. Bioinformatic analysis has demonstrated that MAGOH was frequently overexpressed in multiple tumors compared to adjacent non-cancerous tissues. Moreover, high expression of MAGOH was related to poorer overall survival (OS), disease-specific survival (DSS), disease-free interval (DFI), and progression-free interval (PFI) in certain malignancies, notably an independent prognostic predictor for liver hepatocellular carcinoma (LIHC). Furthermore, MAGOH was closely correlated with immune cell infiltration, immune checkpoint expression, tumor mutational burden (TMB), microsatellite instability (MSI), and mismatch repair (MMR) status. Subsequently, we found that the expression of MAGOH was largely increased in clinical HCC tissues (34/60, 56.7%) compared to non-cancerous tissues. Additionally, MAGOH was positively correlated with advanced TNM staging and vascular invasion. More convincingly, MAGOH upregulation facilitated cell proliferation, migration, and invasion of HCC cells, while MAGOH depletion elicited opposite effects. Collectively, our study conducted a comprehensive analysis of the hitherto undescribed role of MAGOH in pan-cancer by analyzing multi-omics data. More significantly, we recognized MAGOH as a crucial promoter in the malignant progression of hepatocellular carcinoma, providing potential therapeutic targets for HCC patients.
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.