Evolving Molecular Mechanism-Based Strategies for Control of Hepatocellular Carcinoma

Sato, Keiko; Mori, Masataka

doi:10.2174/092986711797200462

Cited by 7 publications

(4 citation statements)

References 140 publications

(181 reference statements)

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“…Other cells in the liver, such as endothelial cells (Sato and Mori 2011) or BM-MSCs (Garcia, et al 2011) may also be altered due to chronic inflammation or tumorigenesis. Ma et al found that infiltration of monocytes/macrophages might alter the growth and invasion patterns of HCC and that targeting AR in HCC might reduce the infiltration of monocytes/macrophages, thereby suppressing monocyte/macrophage-mediated cancer growth (Wen-Lung Ma, Yin- Yi Chen, Chawnshang Chang, 2013).…”

Section: Part II Androgen/ar Signaling In Liver Cancermentioning

confidence: 99%

Androgen receptor roles in hepatocellular carcinoma, fatty liver, cirrhosis and hepatitis

Lung¹,

Lai²,

Yeh³

et al. 2014

Endocrine-Related Cancer

145

114

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Summary Androgen/androgen receptor (AR) signaling plays important roles in normal liver function and in progression of liver diseases. In studies of non-cancerous liver diseases, AR knockout mouse models of liver disease have revealed that androgen/AR signaling suppresses the development of steatosis, virus-related hepatitis, and cirrhosis. In addition, studies have shown that targeting AR in bone marrow-derived mesenchymal stem cells (BM-MSCs) improves their self-renewal and migration potentials, thereby increasing the efficacy of BM-MSC transplantation as a way to control the progression of cirrhosis. Androgen/AR signaling is known to be involved in the initiation of carcinogen- or Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). However, studies have demonstrated that AR, rather than androgen, plays the dominant role in cancer initiation. Therefore, targeting AR might be an appropriate therapy for patients with early-stage HCC. In contrast, androgen/AR signaling has been shown to suppress metastasis of HCC in patients with late-stage disease. In addition, there is evidence that therapy comprising Sorafenib and agents that enhance the functional expression of AR may suppress the progression of late-stage HCC.

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Section: Part II Androgen/ar Signaling In Liver Cancermentioning

confidence: 99%

Androgen receptor roles in hepatocellular carcinoma, fatty liver, cirrhosis and hepatitis

Lung¹,

Lai²,

Yeh³

et al. 2014

Endocrine-Related Cancer

145

114

View full text Add to dashboard Cite

show abstract

“…Although the pathogenesis of HCC has been studied at depth, the exact mechanisms and pathways leading to its development are still unclear [1], [2]. A growing body of literature has demonstrated that aberrant lipid metabolic abnormalities may increase the susceptibility of the liver to tumorigenesis [3], [4].…”

Section: Introductionmentioning

confidence: 99%

Hydroxysteroid Sulfotransferase SULT2B1b Promotes Hepatocellular Carcinoma Cells Proliferation In Vitro and In Vivo

Yang

Guo

et al. 2013

PLoS ONE

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Hydroxysteroid sulfotransferase 2B1b (SULT2B1b) is highly selective for the addition of sulfate groups to 3β-hydroxysteroids. Although previous reports have suggested that SULT2B1b is correlated with cell proliferation of hepatocytes, the relationship between SULT2B1b and the malignant phenotype of hepatocarcinoma cells was not clear. In the present study, we found that SULT2B1 was comparatively higher in the human hepatocarcinoma tumorous tissues than their adjacent tissues. Besides, SULT2B1b overexpression promoted the growth of the mouse hepatocarcinoma cell line Hepa1-6, while Lentivirus-mediated SULT2B1b interference inhibited growth as assessed by the CCK-8 assay. Likewise, inhibition of SULT2B1b expression induced cell-cycle arrest and apoptosis in Hepa1-6 cells by upregulating the expression of FAS, downregulating the expression of cyclinB1, BCL2 and MYC in vitro and in vivo at both the transcript and protein levels. Knock-down of SULT2B1b expression significantly suppressed tumor growth in nude mouse xenografts. Moreover, proliferation rates and SULT2B1b expression were highly correlated in the human hepatocarcinoma cell lines Huh-7, Hep3B, SMMC-7721 and BEL-7402 cells. Knock-down of SULT2B1b inhibited cell growth and cyclinB1 levels in human hepatocarcinoma cells and suppressed xenograft growth in vivo. In conclusion, SULT2B1b expression promotes proliferation of hepatocellular carcinoma cells in vitro and in vivo, which may contribute to the progression of HCC.

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“…Recent studies of patients with liver disease, particularly with HCC, have identified that serum levels of GP73 are more than 30-fold greater than those in patients without the disease (Block et al 2005; Marrero et al 2005). GPC3 is a cell-surface glycoprotein that is absent in the hepatocytes of healthy subjects and patients with hepatitis but highly expressed in hepatocellular cancer cells (Sato and Mori 2011; Jin et al 2012). Several studies have reported that these markers are superior to AFP for the early detection of HCC (Yamamoto et al 2009; Mao et al 2010; Tangkijvanich et al 2010).…”

mentioning

confidence: 99%

Diagnostic Value of Immunohistochemical Staining of GP73, GPC3, DCP, CD34, CD31, and Reticulin Staining in Hepatocellular Carcinoma

Yao

Zhang

Chen

et al. 2013

J Histochem Cytochem.

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It has been reported that Golgi protein-73 (GP73), glypican-3 (GPC3), and des-γ-carboxy prothrombin (DCP) could serve as serum markers for the early detection of hepatocellular carcinoma (HCC). This study aimed to evaluate a panel of immunostaining markers (including GP73, GPC3, DCP, CD34, and CD31) as well as reticulin staining to distinguish HCC from the mimickers. Our results revealed that CD34 immunostaining and reticulin staining were highly sensitive for the diagnosis of HCC. A special immunoreaction pattern of GP73--a diffuse coarse-block pattern in a perinuclear region or a concentrated cluster-like or cord-like pattern in a certain part of the cytoplasm--was observed in HCC cells, in contrast to the cytoplasmic fine-granular pattern in surrounding non-tumor cells and non-malignant nodules. This coarse-block pattern correlated significantly with less differentiated HCC. In comparison, GPC3 displayed a good advantage in diagnosing well-differentiated HCC. In our study, DCP and CD31 showed little diagnostic value for HCC as an immunostaining marker. When GP73, GPC3, and CD34 were combined, the specificity improved to 96.6%. Our findings demonstrate for the first time that the immunohistochemical panel of GP73, GPC3, and CD34 as well as reticulin staining is highly specific for the pathological diagnosis of HCC.

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Evolving Molecular Mechanism-Based Strategies for Control of Hepatocellular Carcinoma

Cited by 7 publications

References 140 publications

Androgen receptor roles in hepatocellular carcinoma, fatty liver, cirrhosis and hepatitis

Androgen receptor roles in hepatocellular carcinoma, fatty liver, cirrhosis and hepatitis

Hydroxysteroid Sulfotransferase SULT2B1b Promotes Hepatocellular Carcinoma Cells Proliferation In Vitro and In Vivo

Diagnostic Value of Immunohistochemical Staining of GP73, GPC3, DCP, CD34, CD31, and Reticulin Staining in Hepatocellular Carcinoma

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