Evidence map›Paper›PMID 39118438›Full record

ArticleCancer reports (Hoboken, N.J.)2024

Deciphering the Molecular Complexity of Hepatocellular Carcinoma: Unveiling Novel Biomarkers and Therapeutic Targets Through Advanced Bioinformatics Analysis.

Ata Moghimi, Nasrin Bani Hosseinian, Mahdi Mahdipour, Ehsan Ahmadpour, Alberto Miranda-Bedate, Saeid Ghorbian

Abstract read
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

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  4. Identification ofTranslational cancer research · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Ata MoghimiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Nasrin Bani HosseinianImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mahdi MahdipourStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ehsan AhmadpourInfectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Alberto Miranda-BedateDepartment of Data Science, EURETOS, Utrecht, The Netherlands.
Saeid GhorbianDepartment of Molecular Genetics, Ahar Branch, Islamic Azad University, Ahar, Iran.ORCID 0000-0003-0780-3159

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) represents a primary liver tumor characterized by a bleak prognosis and elevated mortality rates, yet its precise molecular mechanisms have not been fully elucidated. This study uses advanced bioinformatics techniques to discern differentially expressed genes (DEGs) implicated in the pathogenesis of HCC. The primary objective is to discover novel biomarkers and potential therapeutic targets that can contribute to the advancement of HCC research.

methodsThe bioinformatics analysis in this study primarily utilized the Gene Expression Omnibus (GEO) database as data source. Initially, the Transcriptome analysis console (TAC) screened for DEGs. Subsequently, we constructed a protein-protein interaction (PPI) network of the proteins associated to the identified DEGs with the STRING database. We obtained our hub genes using Cytoscape and confirmed the results through the GEPIA database. Furthermore, we assessed the prognostic significance of the identified hub genes using the GEPIA database. To explore the regulatory interactions, a miRNA-gene interaction network was also constructed, incorporating information from the miRDB database. For predicting the impact of gene overexpression on drug effects, we utilized CANCER DP.

resultsA comprehensive analysis of HCC gene expression profiles revealed a total of 4716 DEGs, consisting of 2430 upregulated genes and 2313 downregulated genes in HCC sample compared to healthy control group. These DEGs exhibited significant enrichment in key pathways such as the PI3K-Akt signaling pathway, nuclear receptors meta-pathway, and various metabolism-related pathways. Further exploration of the PPI network unveiled the P53 signaling pathway and pyrimidine metabolism as the most prominent pathways. We identified 10 hub genes (ASPM, RRM2, CCNB1, KIF14, MKI67, SHCBP1, CENPF, ANLN, HMMR, and EZH2) that exhibited significant upregulation in HCC samples compared to healthy control group. Survival analysis indicated that elevated expression levels of these genes were strongly associated with changes in overall survival in HCC patients. Lastly, we identified specific miRNAs that were found to influence the expression of these genes, providing valuable insights into potential regulatory mechanisms underlying HCC progression.

conclusionThe findings of this study have successfully identified pivotal genes and pathways implicated in the pathogenesis of HCC. These novel discoveries have the potential to significantly enhance our understanding of HCC at the molecular level, opening new ways for the development of targeted therapies and improved prognosis evaluation.

Indexed as

Biomarkers, TumorCarcinoma, HepatocellularComputational BiologyGene Expression ProfilingGene Expression Regulation, NeoplasticGene Regulatory NetworksLiver NeoplasmsProtein Interaction MapsDatabases, GeneticHumansMicroRNAsPrognosisSignal TransductionTranscriptomeBiomarkers, TumorMicroRNAsbioinformaticshepatocellular carcinomahub genesmiRNAs

Identifiers

PMID39118438
PMCPMC11310554

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Registered trials

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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.