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Innovative Therapeutics and Biomarkers in Hepatocellular Carcinoma Research

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 2074

Special Issue Editor


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Guest Editor
Department of Anatomy and Cell Biology, College of Medicine, Gachon University, Incheon, Republic of Korea
Interests: nanomedicine; mesenchymal stem cells; nanoparticles; extracellular vesicles; therapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatocellular carcinoma (HCC) is still a leading cause of cancer that is associated with mortalities. It continues to compel innovations and advancements in biomarker identification and therapeutic approaches. This Special Issue will act as the foundation for innovations made in the field of HCC to address obstacles and challenges of its early diagnosis, effective management, and personalized medicine. We invite original research, systematic reviews, meta-analyses of clinical trials and reviews exploring novel diagnostic biomarkers for early diagnosis and prognosis, along with innovative therapeutics approaches.

This Special Issue aims to foster multidisciplinary and interdisciplinary collaboration among physicians, scientists and manufacturers to improve patient-oriented outcomes and translational research. Submissions highlighting molecular mechanisms, engineering approaches, innovative imaging approaches and AI-driven insights are especially encouraged.

Prof. Dr. Alok Raghav
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hepatocellular carcinoma
  • biomarkers
  • therapeutics
  • imaging
  • artificial intelligence
  • diagnostics

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Published Papers (2 papers)

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Research

28 pages, 20160 KiB  
Article
A Comparative Analysis of the Roles of von Willebrand Factor and ADAMTS13 in Hepatocellular Carcinoma: A Bioinformatics and Microarray-Based Study
by Durmuş Ayan, Şerife Buket Bozkurt Polat, Ergül Bayram, Esma Özmen, Fatma Esin Aydın and Serpil Ersan
Curr. Issues Mol. Biol. 2025, 47(4), 270; https://doi.org/10.3390/cimb47040270 - 10 Apr 2025
Viewed by 281
Abstract
Genetic and epigenetic alterations of various biomolecules at the molecular level can contribute to the pathogenesis of hepatocellular carcinoma (HCC) and negative impact prognosis. In this study, we aimed to investigate the effects of von Willebrand factor (VWF) and ADAMTS13 on HCC prognosis, [...] Read more.
Genetic and epigenetic alterations of various biomolecules at the molecular level can contribute to the pathogenesis of hepatocellular carcinoma (HCC) and negative impact prognosis. In this study, we aimed to investigate the effects of von Willebrand factor (VWF) and ADAMTS13 on HCC prognosis, using bioinformatics tools. “These tools included GEPIA2, TIMER2, UALCAN database, KM-Plotter, TNM-plot, STRING, ENCORI, Human Protein Atlas, Targetscan 8.0, miRDB, Enrichr-KG, lncRNADisease and, GEO”. VWF expression levels were significantly upregulated in liver hepatocellular carcinoma (LIHC) tissues compared to healthy adjacent tissues. Conversely, ADAMTS13 expression levels were significantly downregulated in LIHC tissues compared with healthy adjacent tissues in GEPIA2 database. The upregulated expression of VWF was significantly associated with longer overall survival (OS). However, the downregulated expression of ADAMTS13 was not significantly related to OS. The promoter regions of VWF and ADAMTS13 were significantly hypomethylated. While a significant negative correlation was observed between VWF with CD4 + T cells, there was a positive correlation between VWF with CD8+ T cells. ADAMTS13 expression positively correlated with CD4+ T cells. Additionally, a positive correlation was observed between ADAMTS13 expression and long non-coding RNAs (lncRNAs) (H19, HOTAIR, MALAT1, and UCA1). Conversely, a negative correlation was observed between VWF expression and lncRNAs (H19, HOTAIR, MALAT1, and UCA1). Although these results are promising, they highlight the complexity of the interplay between VWF and ADAMTS13 in HCC progression. According to microarray data, while VWF expression levels were significantly downregulated, ADAMTS13 expression levels were significantly upregulated in HCC compared with the control in the GEO database. Further studies are needed to elucidate the mechanisms underlying these markers. Full article
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25 pages, 6628 KiB  
Article
Dose-Dependent PFESA-BP2 Exposure Increases Risk of Liver Toxicity and Hepatocellular Carcinoma
by Grace Kostecki, Kiara Chuang, Amelia Buxton and Sivanesan Dakshanamurthy
Curr. Issues Mol. Biol. 2025, 47(2), 98; https://doi.org/10.3390/cimb47020098 - 5 Feb 2025
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Abstract
Per- and polyfluoroalkyl substances (PFASs) are persistent and highly bioaccumulative emerging environmental contaminants of concern that display significant toxic and carcinogenic effects. An emerging PFAS is PFESA-BP2, a polyfluoroalkyl ether sulfonic acid found in drinking water and the serum of humans and animals. [...] Read more.
Per- and polyfluoroalkyl substances (PFASs) are persistent and highly bioaccumulative emerging environmental contaminants of concern that display significant toxic and carcinogenic effects. An emerging PFAS is PFESA-BP2, a polyfluoroalkyl ether sulfonic acid found in drinking water and the serum of humans and animals. While PFESA-BP2-induced liver and intestinal toxicity has been demonstrated, the toxicological mechanisms and carcinogenic potential of PFESA-BP2 have remained relatively understudied. Here, we studied how different doses of PFESA-BP2 affect gene activity related to liver toxicity and the risk of liver cancer such as hepatocellular carcinoma (HCC) in mice exposed to PFESA-BP2 once daily through oral gavage for seven days. An analysis of key hepatic pathways suggested increased risk of hepatotoxicity as a result of PFESA-BP2 exposure. Increased oxidative stress response was associated with all concentrations of exposure. Liver toxicity pathways, including PXR/RXR activation and hepatic fibrosis, showed dose-dependent alteration with activation primarily at low doses, suggesting an increased risk of hepatic inflammation and injury. Additionally, an analysis of carcinogenic and HCC-specific pathways suggested PFESA-BP2-induced risk of liver cancer, particularly at low doses. Low-dose PFESA-BP2 exposure (0.03 and 0.3 mg/kg-day) was associated with an increased risk of HCC carcinogenesis, as indicated by the activation of tumor-related and HCC-associated pathways. In contrast, these pathways were inhibited at high doses (3.0 and 6.0 mg/kg-day), accompanied by the activation of HCC-suppressive pathways. The increased risk of HCC development at low doses was mechanistically linked to the activation of signaling pathways such as HIF, EGF, NOTCH4, HGF, and VEGF. Biomarkers linked to liver cancer risk, prognoses, and diagnoses were also identified as a result of exposure. Overall, our findings on liver carcinogenic and hepatotoxic pathway activation patterns suggest that PFESA-BP2 increases the risk of liver toxicity and HCC development, particularly at low doses. Full article
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