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Molecular Research of Hepatocellular Carcinoma
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Molecular Research of Hepatocellular Carcinoma

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 28 June 2024 | Viewed by 2050

Special Issue Editor

Dr. Kuo-Shyang Jeng

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Guest Editor
Department of Surgery, Far Eastern Memorial Hospital, New Taipei City 220, Taiwan
Interests: hepatocellular carcinoma

Special Issue Information

Dear Colleagues,

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide. In spite of the advances of diagnostic tools and various treatments, the disease-free survival rates still remain poor. The etiologies of HCC are very variable, including hepatitis B and C viral infections, excessive alcohol consumption, cigarette smoking, aflatoxin or other environment toxins, nonalcoholic fatty liver disease, other metabolism-related liver diseases, liver fibrosis and cirrhosis, etc. HCC is usually associated with liver inflammation, liver fibrosis and liver cirrhosis. The genomic instability following liver cirrhosis also may affect the development and progression of HCC. The rapid advancement in molecular medicine has led to more detailed dissections of tumor cells and the tumor microenvironment.

Recent studies on HCC are multifactorial. The scopes include numerous interlinked factors, signaling pathways with some processes, novel tumor markers, genetic factors, immunological factors and animal models. These factors or signaling pathways may participate in the carcinogenesis, tumor angiogenesis, tumor invasiveness, cancer progression, cancer recurrence, distant metastasis, extracellular matrix, tumor microenvironment, the initiation and the maintenance of cancer stem cells, resistance to chemotherapy, resistance to various target therapies and radioresistance. However, the intra-tumor heterogeneity contributes to the complexity of the studies and cancer treatments.

In this Special Issue of IJMS, we will focus on the markers and mechanisms contributing to novel treatment strategies which are urgently needed to improve the outcomes of the present treatments. A better understanding needs more advanced studies on HCC.

Research papers and reviews on the abovementioned topics are particularly welcome.

Dr. Kuo-Shyang Jeng
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • liver inflammation
  • signaling pathways
  • novel markers
  • genetic factors
  • target therapies

Published Papers (2 papers)

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Research

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22 pages, 4434 KiB  
Article
Tumor-Extrinsic Axl Expression Shapes an Inflammatory Microenvironment Independent of Tumor Cell Promoting Axl Signaling in Hepatocellular Carcinoma
by Kristina Breitenecker, Denise Heiden, Tobias Demmer, Gerhard Weber, Ana-Maria Primorac, Viola Hedrich, Gregor Ortmayr, Thomas Gruenberger, Patrick Starlinger, Dietmar Herndler-Brandstetter, Iros Barozzi and Wolfgang Mikulits
Int. J. Mol. Sci. 2024, 25(8), 4202; https://doi.org/10.3390/ijms25084202 - 10 Apr 2024
Viewed by 550
Abstract
The activation of the receptor tyrosine kinase Axl by Gas6 is a major driver of tumorigenesis. Despite recent insights, tumor cell-intrinsic and -extrinsic Axl functions are poorly understood in hepatocellular carcinoma (HCC). Thus, we analyzed the cell-specific aspects of Axl in liver cancer [...] Read more.
The activation of the receptor tyrosine kinase Axl by Gas6 is a major driver of tumorigenesis. Despite recent insights, tumor cell-intrinsic and -extrinsic Axl functions are poorly understood in hepatocellular carcinoma (HCC). Thus, we analyzed the cell-specific aspects of Axl in liver cancer cells and in the tumor microenvironment. We show that tumor-intrinsic Axl expression decreased the survival of mice and elevated the number of pulmonary metastases in a model of resection-based tumor recurrence. Axl expression increased the invasion of hepatospheres by the activation of Akt signaling and a partial epithelial-to-mesenchymal transition (EMT). However, the liver tumor burden of Axl+/+ mice induced by diethylnitrosamine plus carbon tetrachloride was reduced compared to systemic Axl−/− mice. Tumors of Axl+/+ mice were highly infiltrated with cytotoxic cells, suggesting a key immune-modulatory role of Axl. Interestingly, hepatocyte-specific Axl deficiency did not alter T cell infiltration, indicating that these changes are independent of tumor cell-intrinsic Axl. In this context, we observed an upregulation of multiple chemokines in Axl+/+ compared to Axl−/− tumors, correlating with HCC patient data. In line with this, Axl is associated with a cytotoxic immune signature in HCC patients. Together these data show that tumor-intrinsic Axl expression fosters progression, while tumor-extrinsic Axl expression shapes an inflammatory microenvironment. Full article
(This article belongs to the Special Issue Molecular Research of Hepatocellular Carcinoma)
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Review

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18 pages, 2019 KiB  
Review
Mechanistic Insights about Sorafenib-, Valproic Acid- and Metformin-Induced Cell Death in Hepatocellular Carcinoma
by Edgar Xchel Franco-Juárez, Vianey González-Villasana, María Elena Camacho-Moll, Luisa Rendón-Garlant, Patricia Nefertari Ramírez-Flores, Beatriz Silva-Ramírez, Katia Peñuelas-Urquides, Ethel Daniela Cabello-Ruiz, Fabiola Castorena-Torres and Mario Bermúdez de León
Int. J. Mol. Sci. 2024, 25(3), 1760; https://doi.org/10.3390/ijms25031760 - 01 Feb 2024
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Abstract
Hepatocellular carcinoma (HCC) is among the main causes of death by cancer worldwide, representing about 80–90% of all liver cancers. Treatments available for advanced HCC include atezolizumab, bevacizumab, sorafenib, among others. Atezolizumab and bevacizumab are immunological options recently incorporated into first-line treatments, along [...] Read more.
Hepatocellular carcinoma (HCC) is among the main causes of death by cancer worldwide, representing about 80–90% of all liver cancers. Treatments available for advanced HCC include atezolizumab, bevacizumab, sorafenib, among others. Atezolizumab and bevacizumab are immunological options recently incorporated into first-line treatments, along with sorafenib, for which great treatment achievements have been reached. However, sorafenib resistance is developed in most patients, and therapeutical combinations targeting cancer hallmark mechanisms and intracellular signaling have been proposed. In this review, we compiled evidence of the mechanisms of cell death caused by sorafenib administered alone or in combination with valproic acid and metformin and discussed them from a molecular perspective. Full article
(This article belongs to the Special Issue Molecular Research of Hepatocellular Carcinoma)
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