Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma

Huaman, Jeannette; Bach, Cuong; Ilboudo, Adeodat; Ogunwobi, Olorunseun O.

doi:10.1007/978-3-319-68082-8_8

Cited by 6 publications

(7 citation statements)

References 140 publications

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“…This process has proved to be involved in various pathological conditions, including inflammation, fibrosis and cancer ( Barriere et al, 2015 ; Skrypek et al, 2017 ). Increasing evidence demonstrated that EMT plays a vital role in transferring malignant hepatocytes during the progression of HCC ( Giannelli et al, 2016 ; Huaman et al, 2018 ; Nitta et al, 2008 ). The association between EMT and HCC raises a demand to exploit novel diagnostic and therapeutic strategies against HCC progression.…”

Section: Discussionmentioning

confidence: 99%

Trends in hepatocellular carcinoma research from 2008 to 2017: a bibliometric analysis

Yan

Zhang

2018

PeerJ

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ObjectivesTo comprehensively analyse the global scientific outputs of hepatocellular carcinoma (HCC) research.MethodsData of publications were downloaded from the Web of Science Core Collection. We used CiteSpace IV and Excel 2016 to analyse literature information, including journals, countries/regions, institutes, authors, citation reports and research frontiers.ResultsUntil March 31, 2018, a total of 24,331 papers in HCC research were identified as published between 2008 and 2017. Oncotarget published the most papers. China contributed the most publications and the United States occupied leading positions in H-index value and the number of ESI top papers. Llovet JM owned the highest co-citations. The keyword “transarterial chemoembolization” ranked first in the research front-line.ConclusionsThe amount of papers published in HCC research has kept increasing since 2008. China showed vast progress in HCC research, but the United States was still the dominant country. Transarterial chemoembolization, epithelial-mesenchymal transition, and cancer stem cell were the latest research frontiers and should be paid more attention.

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Section: Discussionmentioning

confidence: 99%

Trends in hepatocellular carcinoma research from 2008 to 2017: a bibliometric analysis

Yan

Zhang

2018

PeerJ

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“…EMT has been recognized by many in the field to be important for cancer progression[40,41]. In HCC, there have been several reports of EMT effectors such as cadherins, fibronectin, vimentin, and integrins, being altered to permit a more mesenchymal phenotype.…”

Section: Established Biological Mechanisms Of Hcc Progressionmentioning

confidence: 99%

“…Furthermore, transcription factors promoting EMT, including Snail, Slug, Twist and Zeb, are also upregulated during HCC progression[42,43]. Additionally, there have been a number of studies on exosomes, microRNAs, long noncoding RNAs, and regulatory signaling pathways that have been associated with EMT and demonstrate consequences in HCC progression[30,41,44-49]. This is indicative of the important role that EMT plays in HCC progression.…”

Section: Established Biological Mechanisms Of Hcc Progressionmentioning

confidence: 99%

Mechanisms of hepatocellular carcinoma progression

Ogunwobi

Harricharran

Huaman

et al. 2019

WJG

Self Cite

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Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. It is the second leading cause of cancer-related deaths worldwide, with a very poor prognosis. In the United States, there has been only minimal improvement in the prognosis for HCC patients over the past 15 years. Details of the molecular mechanisms and other mechanisms of HCC progression remain unclear. Consequently, there is an urgent need for better understanding of these mechanisms. HCC is often diagnosed at advanced stages, and most patients will therefore need systemic therapy, with sorafenib being the most common at the present time. However, sorafenib therapy only minimally enhances patient survival. This review provides a summary of some of the known mechanisms that either cause HCC or contribute to its progression. Included in this review are the roles of viral hepatitis, non-viral hepatitis, chronic alcohol intake, genetic predisposition and congenital abnormalities, toxic exposures, and autoimmune diseases of the liver. Well-established molecular mechanisms of HCC progression such as epithelial-mesenchymal transition, tumor-stromal interactions and the tumor microenvironment, cancer stem cells, and senescence bypass are also discussed. Additionally, we discuss the roles of circulating tumor cells, immunomodulation, and neural regulation as potential new mechanisms of HCC progression. A better understanding of these mechanisms could have implications for the development of novel and more effective therapeutic and prognostic strategies, which are critically needed.

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“…Upon progression to a high histological grade is accompanied by the loss of normal morphological characteristics, including the E-cadherin whereas the transcription factors associated with EMT such as Snail, Slug, and Twist are increased 248,249 . The expression of mesenchymal proteins correlates with the detection of circulating tumor cells, metastases, and a more aggressive course of the disease 250,251 . EMT induced by IL-6 derived from macrophages that infiltrate the liver tumor promotes the gain of markers of cancer stem cells, invasion, and metastasis.…”

Section: Liver Cancermentioning

confidence: 99%

From Molecular Biology to Epithelial Carcinogenesis

Méndez¹

2021

Preprint

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The theory of the origin of carcinomas suggests that neoplasias from epithelial tissues are the consequence of the reactivation of developmental programs. It proposes a model in which the epithelial cells undergo cellular transitions due to replicative senescence and inflammation towards a mesenchymal-undifferentiated phenotype with cancerous behavior. The conserved pattern of histological progression and the molecular biology of carcinomas is congruent with the view of cancer as a developmental disease. In support of the theory, the experimental literature regarding the molecular, cellular, and histopathological mechanisms associated with epithelial carcinogenesis were aligned according to the premises of the hypothesis. Thereby identified a generic process in the carcinogenesis of the breast, endometrium, prostate, colon, lung, pancreas, bladder, liver, and cervix. Then, is provided a methodology overview of modeling in systems biology derived from previous research testing the hypothesis. The results illustrate the value of the complex systems approach to recover behavior that cannot be inferred only by traditional methods. Specifically, the model suggests that the consistency in the cell types and the directionality of the observed cellular transitions during epithelial carcinogenesis arise from structural constraints in the molecular networks associated with the carcinomas. Overall, the results of the dynamical analysis agree with the premises of the hypothesis and provide an insightful perspective of the potential mechanisms underlying the cellular plasticity displayed during epithelial carcinogenesis. In an era of big data and yet few advances in the underlying causes of chronic diseases, the manuscript also aims to inspire molecular biologists to integrate existing empirical evidence with systems biology modeling in the pursuit of understanding.

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Epithelial-to-Mesenchymal Transition in Hepatocellular Carcinoma

Cited by 6 publications

References 140 publications

Trends in hepatocellular carcinoma research from 2008 to 2017: a bibliometric analysis

Trends in hepatocellular carcinoma research from 2008 to 2017: a bibliometric analysis

Mechanisms of hepatocellular carcinoma progression

From Molecular Biology to Epithelial Carcinogenesis

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