ROS in hepatocellular carcinoma: What we know

Lin, Xiang; Tang, Yu-Ting; Li, Lü; Tao, Xufeng

doi:10.1016/j.abb.2023.109699

Cited by 7 publications

(6 citation statements)

References 191 publications

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“…ROS has dual functions in HCC progression [ 219 ]. Elevated ROS levels in HCC cells facilitate ferroptosis and effectively impede HCC onset and progression [ [220] , [221] , [222] ].…”

Section: Modulation Of Tams By Nanomaterials For Hcc Treatmentmentioning

confidence: 99%

Nanomaterials modulate tumor-associated macrophages for the treatment of digestive system tumors

Li,

Wang,

Yang

et al. 2024

Bioactive Materials

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“…ROS has dual functions in HCC progression [ 219 ]. Elevated ROS levels in HCC cells facilitate ferroptosis and effectively impede HCC onset and progression [ [220] , [221] , [222] ].…”

Section: Modulation Of Tams By Nanomaterials For Hcc Treatmentmentioning

confidence: 99%

Nanomaterials modulate tumor-associated macrophages for the treatment of digestive system tumors

Li,

Wang,

Yang

et al. 2024

Bioactive Materials

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“…Finally, oxidative stress, resulting from the imbalance between the excessive formation of ROS and/or reactive nitrogen species and a reduction in antioxidant defenses, predis-poses cell death and possible tissue damage since ROS contain unpaired electrons, decisive in the abnormal growth and development of cancer cells [223].…”

Section: Mafld and The Development Of Hepatocellular Carcinomamentioning

confidence: 99%

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

De Cól,

de Lima,

Pompeu

et al. 2024

IJMS

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Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain–gut–liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.

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“…NS5A overexpression promotes calcium release from endoplasmatic reticulum (ER), leading to its quick absorption by mitochondria and subsequent elevated production of ROS [84,85]. ROS contributes to carcinogenesis by promoting DNA damage and gene mutation as well as by altering different cell signaling pathways [86]. ROS affect Sp1 (specific protein 1) gene, MDM2 (Mouse double minute 2), p53, and DHCR 24 (3β-hydroxysteroid-∆24 reductase) [86].…”

Section: Oncogenic Signaling Pathwaysmentioning

confidence: 99%

“…ROS contributes to carcinogenesis by promoting DNA damage and gene mutation as well as by altering different cell signaling pathways [86]. ROS affect Sp1 (specific protein 1) gene, MDM2 (Mouse double minute 2), p53, and DHCR 24 (3β-hydroxysteroid-∆24 reductase) [86]. The Sp-family of proteins regulates the expression of genes that play crucial roles in cell proliferation and metastasis of various tumors.…”

Section: Oncogenic Signaling Pathwaysmentioning

confidence: 99%

HCV and HCC Tango—Deciphering the Intricate Dance of Disease: A Review Article

Milosevic,

Todorovic,

Filipovic

et al. 2023

IJMS

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Hepatitis C virus (HCV) is a major cause of hepatocellular carcinoma (HCC) accounting for around one-third of all HCC cases. Prolonged inflammation in chronic hepatitis C (CHC), maintained through a variety of pro- and anti-inflammatory mediators, is one of the aspects of carcinogenesis, followed by mitochondrial dysfunction and oxidative stress. Immune response dysfunction including the innate and adaptive immunity also plays a role in the development, as well as in the recurrence of HCC after treatment. Some of the tumor suppressor genes inhibited by the HCV proteins are p53, p73, and retinoblastoma 1. Mutations in the telomerase reverse transcriptase promoter and the oncogene catenin beta 1 are two more important carcinogenic signaling pathways in HCC associated with HCV. Furthermore, in HCV-related HCC, numerous tumor suppressor and seven oncogenic genes are dysregulated by epigenetic changes. Epigenetic regulation of gene expression is considered as a lasting “epigenetic memory”, suggesting that HCV-induced changes persist and are associated with liver carcinogenesis even after cure. Epigenetic changes and immune response dysfunction are recognized targets for potential therapy of HCC.

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ROS in hepatocellular carcinoma: What we know

Cited by 7 publications

References 191 publications

Nanomaterials modulate tumor-associated macrophages for the treatment of digestive system tumors

Nanomaterials modulate tumor-associated macrophages for the treatment of digestive system tumors

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

HCV and HCC Tango—Deciphering the Intricate Dance of Disease: A Review Article

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