Hepatocellular Carcinoma: Diagnosis and Operative Management

Chedid, Marcio; Kruel, Cléber Rosito Pinto; Pinto, Marcelo Alves; Grezzana-Filho, T.J.M.; Leipnitz, Ian; Kruel, Cléber Dario Pinto; Scaffaro, Leandro Armani; Chedid, Aljamir Duarte

doi:10.1590/0102-6720201700040011

Cited by 75 publications

(54 citation statements)

References 31 publications

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“…The results indicated that NCAPH expression was significantly increased in these datasets (Figure A‐F). The qRT‐PCR results showed that NCAPH expression was significantly higher in HCC tissues than in normal tissues (G). In addition, the IHC results demonstrated that the NCAPH immunostaining signals were stronger in HCC tissues than in adjacent normal liver tissues (ANLTs; Figure A).…”

Section: Resultsmentioning

confidence: 99%

Non‐SMC condensin I complex subunit H enhances proliferation, migration, and invasion of hepatocellular carcinoma

Sun

Huang

Wang

et al. 2019

Molecular Carcinogenesis

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Non‐SMC condensing I complex subunit H (NCAPH) is a member of the Barr protein family and part of the condensin I complex. The upregulation of NCAPH is associated with poor prognosis in patients with colon cancer. However, the relationship between NCAPH and hepatocellular carcinoma (HCC) remains unclear. This study aimed to explore NCAPH expression in HCC tissues and to investigate NCAPH functions in HCC cells. In this study, we found that high expression of NCAPH in HCC indicated worse prognosis via bioinformatics analysis. Consistently, quantitative real‐time polymerase chain reaction assays in 20 pairs of HCC specimens and the immunohistochemical analysis of 100 HCC tissues showed the upregulation of NCAPH. We established stable NCAPH‐overexpressing and NCAPH knockdown cell lines. Cell Counting Kit‐8 assays and colony formation assay were performed to analyze cell proliferation. Migration and invasion were analyzed by Transwell assays. Subcutaneous xenograft models were used to explore the role of NCAPH in tumor formation in vivo. Our results showed that NCAPH promoted tumor proliferation, migration, and invasion in vitro and in vivo. In conclusion, our findings indicate that NCAPH could serve as a novel prognostic biomarker and a potential therapeutic target for patients with HCC.

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Section: Resultsmentioning

confidence: 99%

Non‐SMC condensin I complex subunit H enhances proliferation, migration, and invasion of hepatocellular carcinoma

Sun

Huang

Wang

et al. 2019

Molecular Carcinogenesis

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“…Hepatocellular carcinoma (HCC), as one of the most common cancers, is the leading cause of cancer-associated deaths in China with a characteristic of high morbidity and mortality [1][2][3]. One sorrowful fact about HCC is that the number of HCC patients has been increasing annually.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

2019

Bioscience Reports

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Hepatocellular carcinoma (HCC), as one of the commonest cancers globally, is a primary malignancy in human liver with a characteristic of high mortality rate. Long noncoding RNAs (lncRNAs) are confirmed to be implicated with multiple cancers including HCC. LncRNA FAM83A-AS1 has also been validated as an oncogene in lung cancer, but its mechanism in HCC is poorly understood. Our research is intended to investigate the underlying mechanism of FAM83A-AS1 in HCC. In the present study, we found the abundantly increased expression level of FAM83A-AS1 in HCC tissues and cells. FAM83A-AS1 inhibition hampered cell proliferation, migration and elevated cell apoptosis in HCC. Moreover, FAM83A-AS1 could positively regulate FAM83A, and FAM83A could also promote the progression of HCC. In addition, FAM83A-AS1 and FAM83A were both verified to bind with NOP58, and FAM83A-AS1 enhanced the mRNA stability of FAM83A by binding with NOP58. In rescue assays, the suppressed influence of down-regulated FAM83A-AS1#1 on cell proliferation, migration as well as the accelerated influence of FAM83A-AS1#1 knockdown on cell apoptosis could be partially recovered by overexpression of FAM83A. In conclusion, FAM83A-AS1 facilitated HCC progression by binding with NOP58 to enhance the stability of FAM83A. These findings offer a novel biological insight into HCC treatment.

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“…In this study, 900 patients received surgical treatment for HCC. However, this trial demonstrated that there is no statistical difference in survival between the group of patients receiving sorafenib and the control group [5].…”

mentioning

confidence: 76%

“…Alcohol is also a factor associated with predisposition to liver cirrhosis and, consequently, to HCC, as 80%-90% of patients with HCC have cirrhosis regardless of this etiology [4]. In the United States, alcohol consumption is a relevant risk factor, since the country reports alcohol abuse as a cause related to the development of the disease five times more than hepatitis C [3,5].…”

mentioning

confidence: 99%

Effect of Snake Venom Metalloprotease Desintegrin in Hepatocarcinoma Tumor Cells

Gomes¹,

Gaziola²,

Knop³

et al. 2020

JBTH

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Hepatocellular carcinoma is the third leading cause of cancer-related death in the world. This cancer is associated with cirrhosis following the hepatitis B or C virus infection, alcohol addiction, metabolic liver disease and exposure to dietary toxins such as aflatoxins and aristolochic acid. Studies demonstrate the integration of the HBV genome into liver cell DNA, including cases of patients with HBV-negative serology. Despite advances in prevention techniques, screening, and technology in cancer diagnosis and treatments, the incidence and mortality remain worrisome. Therefore, this research is significant due to the contribution of the development of new biological agents that can be used as monotherapy or adjuvant chemotherapy. Jararhagin, a snake toxin isolated from Bothrops jararaca venom, has been the subject of many studies seeking alternatives for the treatment of cancer. This protein contains the cysteine-rich disintegrin-like metalloproteinase domains and desirable functions to combat tumor cells, such as promoting acute inflammation, damaging the vascular endothelium through the zinc-dependent catalytic domain (responsible for hemorrhagic function) and enzymatically degrading the constituents of the endothelial basement membrane. Due to the antitumor effects of jararhagin presented in previous research, this study aimed to describe the possible antitumor effects of this snake metalloprotease in the murine liver tumor, intending to propose a new therapeutic option in the human liver tumor.

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Hepatocellular Carcinoma: Diagnosis and Operative Management

Cited by 75 publications

References 31 publications

Non‐SMC condensin I complex subunit H enhances proliferation, migration, and invasion of hepatocellular carcinoma

Non‐SMC condensin I complex subunit H enhances proliferation, migration, and invasion of hepatocellular carcinoma

Long noncoding RNA FAM83A-AS1 facilitates hepatocellular carcinoma progression by binding with NOP58 to enhance the mRNA stability of FAM83A

Effect of Snake Venom Metalloprotease Desintegrin in Hepatocarcinoma Tumor Cells

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