Molecular Targets in Hepatocarcinogenesis and Implications for Therapy
1
Department of Emergency Medicine, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 231, Taiwan
2
Department of Emergency Medicine, School of Medicine, Tzu Chi University, Hualien 970, Taiwan
3
Yuh-Ing Junior College of Health Care & Management, Kaohsiung 807, Taiwan
4
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan
5
School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei City 231, Taiwan
6
Department of Pathology, Show Chwan Memorial Hospital, Changhua 500, Taiwan
7
National Institute of Cancer Research, National Health Research Institutes, Miaoli 704, Taiwan
8
Research Assistant Center, Show Chwan Memorial Hospital, Changhua 500, Taiwan
*
Authors to whom correspondence should be addressed.
J. Clin. Med. 2018, 7(8), 213; https://doi.org/10.3390/jcm7080213
Received: 8 July 2018 / Revised: 7 August 2018 / Accepted: 10 August 2018 / Published: 13 August 2018
(This article belongs to the Section Molecular Diagnostics)
Hepatocarcinogenesis comprises of multiple, complex steps that occur after liver injury and usually involve several pathways, including telomere dysfunction, cell cycle, WNT/β-catenin signaling, oxidative stress and mitochondria dysfunction, autophagy, apoptosis, and AKT/mTOR signaling. Following liver injury, gene mutations, accumulation of oxidative stress, and local inflammation lead to cell proliferation, differentiation, apoptosis, and necrosis. The persistence of this vicious cycle in turn leads to further gene mutation and dysregulation of pro- and anti-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-10, IL-12, IL-13, IL-18, and transforming growth factor (TGF)-β, resulting in immune escape by means of the NF-κB and inflammasome signaling pathways. In this review, we summarize studies focusing on the roles of hepatocarcinogenesis and the immune system in liver cancer. In addition, we furnish an overview of recent basic and clinical studies to provide a strong foundation to develop novel anti-carcinogenesis targets for further treatment interventions.
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Keywords:
liver cancer; hepatocarcinogenesis; inflammasome; NF-κB
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
MDPI and ACS Style
Wu, M.-Y.; Yiang, G.-T.; Cheng, P.-W.; Chu, P.-Y.; Li, C.-J. Molecular Targets in Hepatocarcinogenesis and Implications for Therapy. J. Clin. Med. 2018, 7, 213. https://doi.org/10.3390/jcm7080213
AMA Style
Wu M-Y, Yiang G-T, Cheng P-W, Chu P-Y, Li C-J. Molecular Targets in Hepatocarcinogenesis and Implications for Therapy. Journal of Clinical Medicine. 2018; 7(8):213. https://doi.org/10.3390/jcm7080213
Chicago/Turabian StyleWu, Meng-Yu; Yiang, Giuo-Teng; Cheng, Pei-Wen; Chu, Pei-Yi; Li, Chia-Jung. 2018. "Molecular Targets in Hepatocarcinogenesis and Implications for Therapy" J. Clin. Med. 7, no. 8: 213. https://doi.org/10.3390/jcm7080213
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