Molecular Pathogenesis of Hepatocellular Carcinoma

Ho, Daniel Wai‐Hung; Lo, Regina Cheuk‐Lam; Chan, Lap Ki; Ng, Irene Oi–Lin

doi:10.1159/000449340

Cited by 84 publications

(63 citation statements)

References 93 publications

(88 reference statements)

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“…1,2 Its main pathogenic factors include chronic hepatitis B infection, chronic alcohol abuse and non-alcoholic fatty liver disease. 3 Despite advances in the understanding of the molecular mechanisms underlying progression and therapeutic treatments for HCC, the median survival rate remains at approximately 50% (17%-69%) after 5 years. 4 This poor prognosis is mainly led by the frequent intrahepatic or extrahepatic metastasis of HCC.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA LUCAT1 promotes tumourigenesis by inhibiting ANXA2 phosphorylation in hepatocellular carcinoma

Lou

Yu²,

et al. 2018

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNAs) play essential roles in diverse biological processes; however, current understanding of the mechanism underlying the regulation of tumour proliferation and metastasis is limited. Lung cancer‐associated transcript 1 (LUCAT1) has been reported in a variety of human cancers, while its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine the biological role and underlying mechanism of LUCAT1 on progression and metastasis in HCC cells and clinical specimens. Our results demonstrated that LUCAT1 was up‐regulated in HCC tissues and cells. Loss‐ and gain‐of‐function studies revealed that LUCAT1 promotes the proliferation and metastasis of HCC cells in vitro and in vivo. Furthermore, RNA pulldown and Western blot assays indicated that LUCAT1 inhibited the phosphorylation of Annexin A2 (ANXA2) to reduce the degradation of ANXA2‐S100A10 heterotetramer (AIIt), which in turn accelerated the secretion of plasminogen into plasmin, thereby resulting in the activation of metalloprotease proteins. In conclusion, we propose that LUCAT1 serves as a novel diagnostic and therapeutic target for HCC.

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Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA LUCAT1 promotes tumourigenesis by inhibiting ANXA2 phosphorylation in hepatocellular carcinoma

Lou

Yu²,

et al. 2018

J Cellular Molecular Medi

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“…Failure to properly treat AIH and DILI could result in clinically devastating acute or chronic outcomes [5,6] . Chronic AIH could also lead to hepatocarcinogenesis in the future [9][10][11] .…”

mentioning

confidence: 99%

Clinicopathological Study of Autoimmune Hepatitis Cases That Were Difficult to Differentiate from Drug-Induced Liver Injury

Tsutsui¹,

Harada²,

Tsuneyama³

et al. 2017

Dig Dis

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Aim: Acute-onset autoimmune hepatitis (AIH) histopathologically presents with features of acute hepatitis and lacks a specific diagnostic method. Also, AIH is often difficult to differentiate from drug-induced liver injury (DILI). We aimed to investigate the final clinical diagnosis of these cases, and compare the clinical, biochemical, and histological characteristics of AIH vs. DILI. Methods: We examined the Digestive Disease Week Japan 2004 (DDW-J) scale scores, AIH scores, clinical data, and pathological findings in 20 patients in whom it was difficult to differentiate autoimmune liver disease from DILI. Results: In cases with a DDW-J scale score of ≥5, there was a good correlation between the final diagnosis and DDW-J scale assessments, but in cases with a DDW-J scale score of ≦4 they did not correlate well. The scores for pathological findings, such as cobblestone hepatocellular change (p = 0.015), interface hepatitis (p = 0.012), and prominent plasma cells in portal areas (p = 0.011), were higher in the AIH group than in the DILI group. Conclusion: This study showed that DDW-J scale was useful for differentiating AIH from DILI in cases with a DDW-J scale score of ≧5. The histologic features of AIH were characterized by cobblestone hepatocellular change, interface hepatitis, and plasma cell infiltration of the portal region.

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“…[22][23][24][25] Inhibiting these signaling pathways is considered to be an effective method for cancer therapy. [22][23][24][25] Inhibiting these signaling pathways is considered to be an effective method for cancer therapy.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of miR‐623 suppresses progression of hepatocellular carcinoma via regulating the PI3K/Akt signaling pathway by targeting XRCC5

Ren

Jiang

et al. 2019

J of Cellular Biochemistry

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It has been reported that miR‐623 is deregulated in lung adenocarcinoma and inhibits tumor growth and invasion. However, it is unclear whether miR‐623 has a role in the progression of hepatocellular carcinoma (HCC). Herein, we found that miR‐623 was significantly downregulated in HCC, and that its expression was related to poor clinical outcomes of patients with HCC. Upregulation of miR‐623 decreased cell proliferation, viability, migration, and invasion and further promoted apoptosis in 7721, Huh7, and Bel‐7402 cells. Moreover, we also observed that miR‐623 regulated the phosphoinositide 3‐kinase/protein kinase B (PI3K/Akt), Wnt/β‐catenin, and extracellular regulated protein kinases/c‐Jun N‐terminal kinase (ERK/JNK) signaling pathways as well as the expression level of related proteins. Further, X‐ray repair cross complementing 5 (XRCC5) was a direct target for miR‐623, and the suppression of PI3K/Akt, Wnt/β‐catenin, and ERK/JNK signaling pathways and cell proliferation and invasion abilities caused by miR‐623 in HCC cells was significantly reversed by the upregulation of XRCC5. Collectively, our data suggested that miR‐623 suppressed the progression of HCC by regulating the PI3K/Akt, Wnt/β‐catenin, and ERK/JNK pathways by targeting XRCC5 in HCC in vitro, indicating that miR‐623 may be a target for the therapy of HCC.

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Molecular Pathogenesis of Hepatocellular Carcinoma

Cited by 84 publications

References 93 publications

Long non‐coding RNA LUCAT1 promotes tumourigenesis by inhibiting ANXA2 phosphorylation in hepatocellular carcinoma

Long non‐coding RNA LUCAT1 promotes tumourigenesis by inhibiting ANXA2 phosphorylation in hepatocellular carcinoma

Clinicopathological Study of Autoimmune Hepatitis Cases That Were Difficult to Differentiate from Drug-Induced Liver Injury

Overexpression of miR‐623 suppresses progression of hepatocellular carcinoma via regulating the PI3K/Akt signaling pathway by targeting XRCC5

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