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Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment 2.0
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Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 16 June 2024 | Viewed by 2681

Special Issue Editors

Dr. Cristian Turato

E-Mail Website
Guest Editor
Department of Molecular Medicine, University of Pavia, 27100 Pavia, Italy
Interests: liver cancer; liver fibrosis; NASH; liver signalling; liver models of disease; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Stefania Cannito

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, University of Torino, 10125 Torino, Italy
Interests: liver disease; cancer research; liver fibrosis; metabolism and liver; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hepatocellular carcinoma (HCC) remains a global health challenge and its incidence is growing worldwide. It is estimated that, by 2025, >1 million individuals will be affected by liver cancer annually. Studies using next-generation sequencing suggest different patterns of HCC evolution and confirm the high molecular heterogeneity in a subset of patients. Moreover, data indicate a fundamental contribution of nonmalignant cells of the tumour microenvironment to cancer clonal evolution. Delineating these dynamics is crucial to improving the treatment of HCC, and particularly to help understand how HCC evolution drives resistance to systemic therapies. Currently, potentially systemic therapies, including immune checkpoint inhibitors, tyrosine kinase inhibitors and monoclonal antibodies, have challenged the use of conventional therapies for HCC. Approximately 50% of patients with HCC are estimated to be exposed to systemic therapies in their lifespan, particularly in advanced stages of the disease, and biomarker-based stratification of patients for optimal response to therapy is an unmet need.

In this Special Issue, I invite you to contribute original and cutting-edge research articles, reviews related to the theme of “Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment 2.0”.

More published papers could be found in the closed Special Issue: Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment.

Dr. Cristian Turato
Dr. Stefania Cannito
Guest Editors

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

  • human hepatocellular carcinoma (HCC)
  • tumour microenvironment
  • biomarkers
  • immunotherapy
  • epigenetic modulators
  • precise medicine
  • combination strategies

Published Papers (2 papers)

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Research

16 pages, 2536 KiB  
Article
All Three AKT Isoforms Can Upregulate Oxygen Metabolism and Lactate Production in Human Hepatocellular Carcinoma Cell Lines
by Ling-Yu Tian, Daniel J. Smit, Nadezhda V. Popova, Stefan Horn, Lis Noelia Velasquez, Samuel Huber and Manfred Jücker
Int. J. Mol. Sci. 2024, 25(4), 2168; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25042168 - 11 Feb 2024
Viewed by 1073
Abstract
Hepatocellular carcinoma (HCC), the main pathological type of liver cancer, is related to risk factors such as viral hepatitis, alcohol intake, and non-alcoholic fatty liver disease (NAFLD). The constitutive activation of the PI3K/AKT signaling pathway is common in HCC and has essential involvement [...] Read more.
Hepatocellular carcinoma (HCC), the main pathological type of liver cancer, is related to risk factors such as viral hepatitis, alcohol intake, and non-alcoholic fatty liver disease (NAFLD). The constitutive activation of the PI3K/AKT signaling pathway is common in HCC and has essential involvement in tumor progression. The serine/threonine kinase AKT has several downstream substrates, which have been implicated in the regulation of cellular metabolism. However, the contribution of each of the three AKT isoforms, i.e., AKT1, AKT2 and AKT3, to HCC metabolism has not been comprehensively investigated. In this study, we analyzed the functional role of AKT1, AKT2 and AKT3 in HCC metabolism. The overexpression of activated AKT1, AKT2 and AKT3 isoforms in the human HCC cell lines Hep3B and Huh7 resulted in higher oxygen consumption rate (OCR), ATP production, maximal respiration and spare respiratory capacity in comparison to vector-transduced cells. Vice versa, lentiviral vector-mediated knockdowns of each AKT isoform reduced OCR in both cell lines. Reduced OCR rates observed in the three AKT isoform knockdowns were associated with reduced extracellular acidification rates (ECAR) and reduced lactate production in both analyzed cell lines. Mechanistically, the downregulation of OCR by AKT isoform knockdowns correlated with an increased phosphorylation of the pyruvate dehydrogenase on Ser232, which negatively regulates the activity of this crucial gatekeeper of mitochondrial respiration. In summary, our data indicate that each of the three AKT isoforms is able to upregulate OCR, ECAR and lactate production independently of each other in human HCC cells through the regulation of the pyruvate dehydrogenase. Full article
(This article belongs to the Special Issue Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment 2.0)
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16 pages, 4340 KiB  
Article
Unraveling the Role of RNA-Binding Proteins, with a Focus on RPS5, in the Malignant Progression of Hepatocellular Carcinoma
by Chongyang Zhou, Qiumin Wu, Haibei Zhao, Ruixi Xie, Xin He and Huiying Gu
Int. J. Mol. Sci. 2024, 25(2), 773; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25020773 - 07 Jan 2024
Viewed by 1043
Abstract
Hepatocellular carcinoma (HCC) represents a major global health concern, demanding a thorough understanding of its molecular mechanisms for effective therapeutic strategies. RNA-binding proteins (RBPs) play critical roles in post-transcriptional gene regulation, with their dysregulation increasingly recognized as a hallmark of various cancers. However, [...] Read more.
Hepatocellular carcinoma (HCC) represents a major global health concern, demanding a thorough understanding of its molecular mechanisms for effective therapeutic strategies. RNA-binding proteins (RBPs) play critical roles in post-transcriptional gene regulation, with their dysregulation increasingly recognized as a hallmark of various cancers. However, the specific contributions of RBPs to HCC pathogenesis and prevention remain incompletely understood. In this study, we systematically conducted an examination of the expression profiles and clinical relevance of RBPs in 556 clinical samples from well-established cohorts. Through comprehensive analyses, a subset of RBPs exhibiting significant overexpression in HCC was identified, establishing a noteworthy correlation between their aberrant expression and HCC progression. Furthermore, 40S ribosomal protein S5 (RPS5), a ribosomal protein, emerged as a potential key contributor in HCC progression. Rigorous analyses established a correlation between elevated RPS5 expression and advanced clinicopathological features, suggesting its potential as a prognostic biomarker. Experiments further confirmed the impact of RPS5 on pivotal cellular processes implicated in cancer progression, including cell proliferation and metastasis. Further mechanistic studies unveiled the potential of RPS5 to activate the cell cycle by binding to key molecules involved in the pathway, thereby promoting the malignant progression of HCC. Additionally, our analysis of the etiology behind RPS5 overexpression in HCC posited it as an outcome of transcriptional regulation by the transcription factors Nuclear Respiratory Factor 1 (NRF1) and MYC-associated zinc finger protein (MAZ). In conclusion, our study contributes to the growing evidence elucidating the intricate involvement of RBPs, exemplified by RPS5, in the malignant progression of HCC. The integration of genomic, transcriptomic, and functional analyses provides a comprehensive understanding of the regulatory mechanisms associated with RPS5 in HCC. This comprehensive analysis not only advances our knowledge of the molecular drivers behind HCC but also highlights the potential therapeutic relevance of targeting RBPs and their regulatory network for the development of more effective treatment strategies. Full article
(This article belongs to the Special Issue Hepatocellular Carcinoma: Latest Research in Pathogenesis, Detection and Treatment 2.0)
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