JAK/STAT signaling in hepatocellular carcinoma

Tang, Justin Jit Hin; Thng, Dexter Kai Hao; Lim, Jackwee; Toh, Tan Boon

doi:10.2217/hep-2020-0001

Cited by 104 publications

(59 citation statements)

References 102 publications

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“…The signal transducer and activator of transcription (STAT) protein family has seven members, STAT1-5, STAT5B, and STAT6 [ 135 , 136 ]. STAT3 has been found to be involved in promoting HCC development and malignant and cancer stemness characteristics [ 134 , 135 , 137 , 138 , 139 ]. When IGF/IGF-1R signaling was deactivated by miR-486-5p or siRNA-IGF-1R, the levels of STAT3, mTOR, and cMyc were reduced, and colony formation was suppressed [ 140 ].…”

Section: Igf/igf-1 Signaling In Hccmentioning

confidence: 99%

The Role of IGF/IGF-1R Signaling in Hepatocellular Carcinomas: Stemness-Related Properties and Drug Resistance

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Jeng

Kuo

et al. 2021

IJMS

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Insulin-like Growth Factor (IGF)/IGF-1 Receptor (IGF-1R) signaling is known to regulate stem cell pluripotency and differentiation to trigger cell proliferation, organ development, and tissue regeneration during embryonic development. Unbalanced IGF/IGF-1R signaling can promote cancer cell proliferation and activate cancer reprogramming in tumor tissues, especially in the liver. Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death, with a high incidence and mortality rate in Asia. Most patients with advanced HCC develop tyrosine kinase inhibitor (TKI)-refractoriness after receiving TKI treatment. Dysregulation of IGF/IGF-1R signaling in HCC may activate expression of cancer stemness that leads to TKI refractoriness and tumor recurrence. In this review, we summarize the evidence for dysregulated IGF/IGF-1R signaling especially in hepatitis B virus (HBV)-associated HCC. The regulation of cancer stemness expression and drug resistance will be highlighted. Current clinical treatments and potential therapies targeting IGF/IGF-1R signaling for the treatment of HCC will be discussed.

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Section: Igf/igf-1 Signaling In Hccmentioning

confidence: 99%

The Role of IGF/IGF-1R Signaling in Hepatocellular Carcinomas: Stemness-Related Properties and Drug Resistance

Ngo

Jeng

Kuo

et al. 2021

IJMS

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“…It is thus conceivable that persistent HCV-induced signaling alterations and deranged cytokine production may promote the development of extrahepatic manifestations in immune cells [148]. Several compounds targeting these signaling pathways have been suggested for chemoprevention of HCC (reviewed in detail in [149,150]) and targeting HCV-relevant pathways to treat established HCC have been suggested [151][152][153]. Therefore, learning from HCV-induced liver disease will help to develop novel diagnostics and personalized therapeutic concepts that may be useful to prevent and potentially also to treat HCC from other related liver disease etiologies like NAFLD.…”

Section: Clinical Implications For Biomarker Discovery To Predict Hcvmentioning

confidence: 99%

Hepatitis C Virus and Hepatocellular Carcinoma: When the Host Loses Its Grip

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Suarez

Wrensch

et al. 2020

IJMS

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Chronic infection with hepatitis C virus (HCV) is a major cause of hepatocellular carcinoma (HCC). Novel treatments with direct-acting antivirals achieve high rates of sustained virologic response; however, the HCC risk remains elevated in cured patients, especially those with advanced liver disease. Long-term HCV infection causes a persistent and accumulating damage of the liver due to a combination of direct and indirect pro-oncogenic mechanisms. This review describes the processes involved in virus-induced disease progression by viral proteins, derailed signaling, immunity, and persistent epigenetic deregulation, which may be instrumental to develop urgently needed prognostic biomarkers and as targets for novel chemopreventive therapies.

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“…The JAK/STAT signaling pathway plays crucial roles in many cell progresses, including cell proliferation and immune response. Many studies have reported that JAK/STAT signaling is aberrantly activated in HCC and activated JAK/STAT pathway causes dysregulation of its many downstream target genes correlated with proliferation, immune, invasion, and metastasis [ 18 , 19 ]. In addition, hepcidin activates the JAK/STAT pathway through Jak2 activation and transcription factor Stat3 phosphorylation [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

The Effects of Dandelion Polysaccharides on Iron Metabolism by Regulating Hepcidin via JAK/STAT Signaling Pathway

Ren

Yang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Recent studies have claimed that iron overload was correlated with the risk of hepatocellular carcinoma (HCC), and our previous studies have also demonstrated that dandelion polysaccharide (DP) suppressed HCC cell line proliferation via causing cell cycle arrest and inhibiting the PI3K/AKT/mTOR pathway, but the effect of DP on metabolism is still not very clear. Here, we aim to clarify the effects of DP on iron metabolism and the underlying mechanism. In this study, we found that DP could reduce iron burden in hepatoma cells and grafted tumors. Hepcidin is a central regulator in iron metabolism. We confirmed that the expression of hepcidin in HCC tumor tissues was significantly higher than that in the adjacent nontumor tissues. The expression of hepcidin was downregulated in the liver of mouse model treatment with DP, as well as in hepatoma cells. Moreover, RNA sequencing and western blot data revealed that DP inhibited the IL-6-activated JAK-STAT signaling pathway. In summary, our results revealed that DP might be a new potential drug candidate for the regulation of iron burden and the treatment of HCC.

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JAK/STAT signaling in hepatocellular carcinoma

Cited by 104 publications

References 102 publications

The Role of IGF/IGF-1R Signaling in Hepatocellular Carcinomas: Stemness-Related Properties and Drug Resistance

The Role of IGF/IGF-1R Signaling in Hepatocellular Carcinomas: Stemness-Related Properties and Drug Resistance

Hepatitis C Virus and Hepatocellular Carcinoma: When the Host Loses Its Grip

The Effects of Dandelion Polysaccharides on Iron Metabolism by Regulating Hepcidin via JAK/STAT Signaling Pathway

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