Evidence map›Paper›PMID 39671369›Full record

ArticlePloS one2024

Comprehensive analysis of bioinformatics and system biology reveals the association between Girdin and hepatocellular carcinoma.

Tengda Huang, Hongying Chen, Hongyuan Pan, Tian Wu, Xiangyi Ren, Liwen Qin, Kefei Yuan, Fang He

Erratum issuedAbstract read
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Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Tengda HuangDivision of Liver Surgery, Department of General Surgery and Laboratory of Liver Surgery, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-4056-7584
Hongying ChenCytology and Molecular Platform, Core Facilities of West China Hospital, Chengdu, China.
Hongyuan PanDivision of Liver Surgery, Department of General Surgery and Laboratory of Liver Surgery, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Tian WuNHC Key Laboratory of Transplant Engineering and Immunology, Regenerative Medicine Research Center, Frontiers Science Center for Disease-related Molecular Network, West China Hospital of Sichuan University, Chengdu, China.
Xiangyi RenCenter of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China.
Liwen QinCenter of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China.
Kefei YuanDivision of Liver Surgery, Department of General Surgery and Laboratory of Liver Surgery, and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Fang HeCenter of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0002-1024-5736

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionHepatocellular carcinoma is one of the leading causes of cancer-related mortality worldwide. The actin-binding protein Girdin is overexpressed in various tumors, promoting tumorigenesis and progression. However, the exact mechanisms by which Girdin regulates liver cancer remain poorly understood.

methodsThis study comprehensively analyzed the expression level of Girdin in liver cancer and adjacent tissue, along with the correlation between Girdin expression and the clinical characteristics and prognosis of liver cancer. The analysis integrated data from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO), and Clinical Proteomic Tumor Analysis Consortium (CPTAC) database. Subsequently, Girdin expression was knocked down to elucidate its role in the progression of liver cancer. Transcriptome sequencing was employed to investigate the mechanistic underpinnings of Girdin's regulatory impact on liver cancer. Additionally, the Comparative Toxicogenomics Database (CTD) was utilized to identify potential drugs or molecules for liver cancer treatment.

resultsThe findings revealed elevated Girdin expression in liver cancer tissues, and heightened Girdin expression correlating with adverse clinical features and prognosis. Silencing of Girdin markedly impeded the proliferation and migration of hepatocellular carcinoma cells. Moreover, transcriptome sequencing demonstrated that silencing Girdin led to differential expression of 176 genes and inhibition of the PI3K/Akt signaling pathway, as well as its upstream pathways-Cytokine-cytokine receptor interaction and Chemokine signaling pathway. Ultimately, we propose that Imatinib Mesylate, Orantinib, Resveratrol, Sorafenib, and Curcumin may interact with Girdin, potentially contributing to the treatment of liver cancer.

conclusionThis study reveals the association between Girdin and hepatocellular carcinoma, providing novel clues for future research and treatment of hepatocellular carcinoma.

Indexed as

Carcinoma, HepatocellularComputational BiologyGene Expression Regulation, NeoplasticLiver NeoplasmsMicrofilament ProteinsVesicular Transport ProteinsCell Line, TumorCell MovementCell ProliferationHumansMalePrognosisSignal TransductionSystems BiologyCCDC88A protein, humanMicrofilament ProteinsVesicular Transport Proteins

Identifiers

PMID39671369
PMCPMC11642971

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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.