دورية أكاديمية

Oxidative stress in obesity-associated hepatocellular carcinoma: sources, signaling and therapeutic challenges.

التفاصيل البيبلوغرافية
العنوان: Oxidative stress in obesity-associated hepatocellular carcinoma: sources, signaling and therapeutic challenges.
المؤلفون: Brahma MK; Signal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium., Gilglioni EH; Signal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium., Zhou L; Materials Research and Education Center, Auburn University, Auburn, AL, 36849, United States., Trépo E; Department of Gastroenterology, Hepatopancreatology and Digestive Oncology, C.U.B. Hôpital Erasme, Université libre de Bruxelles, Brussels, Belgium.; Laboratory of Experimental Gastroenterology, Université libre de Bruxelles, Brussels, Belgium., Chen P; Materials Research and Education Center, Auburn University, Auburn, AL, 36849, United States., Gurzov EN; Signal Transduction and Metabolism Laboratory, Laboratoire de Gastroentérologie Expérimental et Endotools, Université libre de Bruxelles, Brussels, Belgium. esteban.gurzov@ulb.be.
المصدر: Oncogene [Oncogene] 2021 Aug; Vol. 40 (33), pp. 5155-5167. Date of Electronic Publication: 2021 Jul 21.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5594 (Electronic) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene
أسماء مطبوعة: Publication: <2002->: Basingstoke : Nature Publishing Group
Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987-
مواضيع طبية MeSH: Carcinoma, Hepatocellular*/metabolism , Carcinoma, Hepatocellular*/etiology , Carcinoma, Hepatocellular*/pathology , Liver Neoplasms*/metabolism , Liver Neoplasms*/pathology , Liver Neoplasms*/etiology , Liver Neoplasms*/genetics , Obesity*/complications , Obesity*/metabolism , Oxidative Stress* , Signal Transduction* , Reactive Oxygen Species*/metabolism, Humans ; Animals
مستخلص: Obesity affects more than 650 million individuals worldwide and is a well-established risk factor for the development of hepatocellular carcinoma (HCC). Oxidative stress can be considered as a bona fide tumor promoter, contributing to the initiation and progression of liver cancer. Indeed, one of the key events involved in HCC progression is excessive levels of reactive oxygen species (ROS) resulting from the fatty acid influx and chronic inflammation. This review provides insights into the different intracellular sources of obesity-induced ROS and molecular mechanisms responsible for hepatic tumorigenesis. In addition, we highlight recent findings pointing to the role of the dysregulated activity of BCL-2 proteins and protein tyrosine phosphatases (PTPs) in the generation of hepatic oxidative stress and ROS-mediated dysfunctional signaling, respectively. Finally, we discuss the potential and challenges of novel nanotechnology strategies to prevent ROS formation in obesity-associated HCC.
(© 2021. The Author(s), under exclusive licence to Springer Nature Limited.)
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معلومات مُعتمدة: R35 GM133795 United States GM NIGMS NIH HHS
المشرفين على المادة: 0 (Reactive Oxygen Species)
تواريخ الأحداث: Date Created: 20210722 Date Completed: 20240724 Latest Revision: 20240724
رمز التحديث: 20240726
مُعرف محوري في PubMed: PMC9277657
DOI: 10.1038/s41388-021-01950-y
PMID: 34290399
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5594
DOI:10.1038/s41388-021-01950-y