Bioinformatics analysis of hepatitis C virus genotype 2a-induced human hepatocellular carcinoma in Huh7 cells
Open accessAbstract
Hepatocellular carcinoma (HCC) is a liver cancer that could be induced by hepatitis C virus genotype 2a Japanese fulminant hepatitis-1 (JFH-1) strain. The aim of this study was to investigate the molecular mechanisms of HCC. The microarray data GSE20948 includes 14 JFH-1- and 14 mock (equal volume of medium [control])-infected Huh7 samples. The data were downloaded from the Gene Expression Omnibus. After data processing, soft cluster analyses were performed to identify co-regulated genes with similar temporal expression patterns. Functional and pathway enrichment analyses, as well as functional annotation analysis, were performed. Subsequently, combined networks of protein-protein interaction network, microRNA regulatory network, and transcriptional regulatory network were constructed. Hub nodes, modules, and five clusters of co-regulated genes were also identified. In total, 173 up and 207 down co-regulated genes were separately identified in JFH-1-infected Huh7 cells compared with those of control cells. Functional enrichment analysis indicated that up co-regulated genes were related to skeletal system morphogenesis and neuron differentiation and down co-regulated genes were related to steroid/cholesterol/sterol metabolisms. Hub genes (such as IRF1, GBP1, ICAM1, Foxa1, DHCR7, HMGCS2, and MSMO1) were identified. Transcription factors IRF1 and Foxa1 were the targets of miR-130a, miR-17-5p, and miR-20a. PPARGC1A was targeted by miR-29 family, and MSMO1 was the target of miR-23 family. Hub nodes (such as IRF1, GBP1, ICAM1, Foxa1, DHCR7, HMGCS2, and MSMO1) and microRNAs might be used as candidate biomarkers of JFH-1-infected HCC.
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In HCC patients induced by hepatitis C virus genotype 2a JFH-1, MSMO1 is a target of the miR-23 family.
“the low-expression differentially expressed gene MSMO1 is a target of the miR-23 family.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [74]
The Results ('Combination of the networks') identify MSMO1 as a down-regulated gene targeted by miR-23a and miR-23b, supporting the citing sentence. But the study’s JFH-1 comparison used infected Huh7 cells, not patients with genotype 2a-induced HCC; the patient-specific framing is not established by these passages. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn HBV-infected HCC patients, miR-23a is decreased and target gene CCL22 is increased.
“miR-23a decreased in HCC patients infected with the hepatitis B virus, along with an increase in the target gene CCL22.”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [74]
The Conclusion (page unavailable) identifies MSMO1 as a target of miR-23a in a hepatitis C virus–infected Huh7 cell analysis. Searches for HBV-infected HCC patients, decreased miR-23a, and increased CCL22 found no passage addressing the claimed patient finding. (LLM, conf=0.76)
Experimental — accuracy not yet measuredmiR-23a inhibitors promote tumor growth by upregulating CCL22 on the p65/miR-23a/CCL22 axis to regulate T cell recruitment in HBV-positive HCC.
“The use of miR-23a inhibitors promotes tumor growth by upregulating target gene CCL22 on the p65/miR-23a/CCL22 axis to regulate T cell recruitment in hepatitis B virus positive HCC [74,75].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [74]
The Results and Conclusion (pages not provided) identify MSMO1 as a predicted target of miR-23a in HCV-related HCC. A search for CCL22, p65, T-cell recruitment, HBV, and miR-23a inhibitors found no passage addressing the claimed mechanism or tumor-growth effect. (LLM, conf=0.76)
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He, W., Tian, Z., Dong, B., Cao, Y., Hu, W., Wu, P., Yu, L., Zhang, X., & Guo, S. (2024) · Figshare · doi:10.6084/m9.figshare.25374756
- Authors
- Xu, J., Xu, P., Wu, M., Chen, H., Xu, J., Wu, M., Li, M., & Qian, F.
- Affiliations
- Soochow University (CN)
- Corresponding author
- Xu, Junhua
- Venue
- OncoTargets and Therapy
- Publisher
- Informa UK Limited
- Published
- 2016-01
- Volume
- 9
- Pages
- 191
- ISSN
- 1178-6930 (ISSN-L)
- PMC
- PMC4712971
- OpenAlex
- W2228800533
- Cited by
- 20
- References
- 69
- Citations by year
- 2025: 1 · 2024: 6 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 3 · 2018: 2 · 2016: 2
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- OncoTargets and Therapy (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Topics
- Health Sciences › Medicine › Hepatology › Hepatitis C virus research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioinformatics and Genomic Networks
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Keywords
- JFH1, hepatocellular carcinoma, Huh7 cells, gene expression profiling, co-regulated genes, hub genes, miRNA regulatory network, transcriptional regulatory networks, protein-protein interaction network, IRF1, FOXA1, miR-130a, miR-17-5p, miR-20a, miR-29 family, PGC-1α, biomarkers
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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