Evaluation of glioma-associated oncogene 1 expression and its correlation with the expression of sonic hedgehog, E-cadherin and S100a4 in human hepatocellular carcinoma

Zheng, Xin; Yao, Yingmin; Xu, Qiuran; Tu, Kangsheng; Liu, Qingguang

doi:10.3892/mmr.2010.375

Cited by 16 publications

(14 citation statements)

References 12 publications

(12 reference statements)

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“…The cell apoptosis in the xenograft tissues was measured by TUNEL assay according to the manufacturer’s guidelines. The details of IHC protocal have been described previously [22]. …”

Section: Methodsmentioning

confidence: 99%

Histone acetyltransferase PCAF Up-regulated cell apoptosis in hepatocellular carcinoma via acetylating histone H4 and inactivating AKT signaling

et al. 2013

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BackgroundPCAF is an important intrinsic histone acetyltransferases. This study tried to establish the effect of PCAF on HCC cell apoptosis.MethodBoth in vitro and in vivo experiments including IHC, DAPI staining, caspase 3/7 activity assay, BrdU assay, MTT assay, western immunoblotting and co-immunoprecipitation were used here.ResultsPCAF was found to be expressed at the low level in most of HCC cell lines. PCAF overexpression induced cell apoptosis and growth arrest with increased Histone H4 acetylation and inactivation of AKT signaling in Huh7 and HepG2 cells. The opposite results were obtained by silencing PCAF in Hep3B cells. The co-immunoprecipitation assay confirmed that PCAF protein was bound with histone H4 protein in the nucleus of Hep3B cells. Finally, the in vivo experiment confirmed the findings mentioned-above.ConclusionThese data identified PCAF promotes cell apoptosis and functions as a HCC repressor through acetylating histone H4 and inactivating AKT signaling.

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“…The cell apoptosis in the xenograft tissues was measured by TUNEL assay according to the manufacturer’s guidelines. The details of IHC protocal have been described previously [22]. …”

Section: Methodsmentioning

confidence: 99%

Histone acetyltransferase PCAF Up-regulated cell apoptosis in hepatocellular carcinoma via acetylating histone H4 and inactivating AKT signaling

et al. 2013

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“…A line of evidences have revealed that EMT modulates malignant characteristics of cancer cells such as mobility, invasion, anti-apoptosis and stem-liking phenotypes[23]. Our previous studies showed that EMT appeared frequently in HCC and was involved in increased migration and invasion ability of HCC cells[24], [25]. In addition, we demonstrated that GLI1 overexpression was responsible for EMT phenotype of HCC and indispensable for TGFβ1-driven EMT of HCC cells[24].…”

Section: Introductionmentioning

confidence: 72%

“…IHC staining was performed as described previously[25]. Briefly speaking, the paraffin slides were dewaxed and dehydrated.…”

Section: Methodsmentioning

confidence: 99%

Caveolin-1 Is Up-Regulated by GLI1 and Contributes to GLI1-Driven EMT in Hepatocellular Carcinoma

Gai

et al. 2014

PLoS ONE

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Caveolin-1 (Cav-1) has been recently identified to be over-expressed in hepatocellular carcinoma (HCC) and promote HCC cell motility and invasion ability via inducing epithelial-mesenchymal transition (EMT). However, the mechanism of aberrant overexpression of Cav-1 remains vague. Here, we observed that Cav-1 expression was positively associated with GLI1 expression in HCC tissues. Forced expression of GLI1 up-regulated Cav-1 in Huh7 cells, while knockdown of GLI1 decreased expression of Cav-1 in SNU449 cells. Additionally, silencing Cav-1 abolished GLI1-induced EMT of Huh7 cells. The correlation between GLI1 and Cav-1 was confirmed in tumor specimens from HCC patients and Cav-1 was found to be associated with poor prognosis after hepatic resection. The relationship between protein expression of GLI1 and Cav-1 was also established in HCC xenografts of nude mice. These results suggest that GLI1 may be attributed to Cav-1 up-regulation which plays an important role in GLI1-driven EMT phenotype in HCC.

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“…Zheng et al . found that Gli1 protein expression was positively correlated with Shh and S100a4, and negatively correlated with E-cadherin [42]. EMT is regulated by several transcription factors, including Snail, ZEB1, ZEB2, Twist1, and Twist2, each of which bind to the E-cadherin promoter region and repress its transcription [43-49].…”

Section: Discussionmentioning

confidence: 99%

Expression of glioma-associated oncogene 2 (Gli 2) is correlated with poor prognosis in patients with hepatocellular carcinoma undergoing hepatectomy

Zhang

Cao

et al. 2013

World J Surg Onc

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BackgroundOur previous studies showed that glioma-associated oncogene (Gli)2 plays an important role in the proliferation and apoptosis resistance of hepatocellular carcinoma (HCC) cells. The aim of this study was to explore the clinical significance of Gli2 expression in HCC.MethodsExpression of Gli2 protein was detected in samples from 68 paired HCC samples, the corresponding paraneoplastic liver tissues, and 20 normal liver tissues using immunohistochemistry. Correlation of the immunohistochemistry results with clinicopathologic parameters, prognosis, and the expression of E-cadherin, N-cadherin, and vimentin were analyzed.ResultsImmunohistochemical staining showed high levels of Gli2 protein expression in HCC, compared with paraneoplastic and normal liver tissues (P < 0.05). This high expression level of Gli2 was significantly associated with tumor differentiation, encapsulation, vascular invasion, early recurrence, and intra-hepatic metastasis (P < 0.05). There was a significantly negative correlation between Gli2 and E-cadherin expression (r = −0.302, P < 0.05) and a significantly positive correlation between expression of Gli2 and expression of vimentin (r = −0.468, P < 0.05) and N-cadherin (r = −0.505, P < 0.05). Kaplan-Meier analysis showed that patients with overexpressed Gli2 had significantly shorter overall survival and disease-free survival times (P < 0.05). Multivariate analysis suggested that the level of Gli2 expression was an independent prognostic factor for HCC.ConclusionsExpression of Gli2 is high in HCC tissue, and is associated with poor prognosis in patients with HCC after hepatectomy.

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Evaluation of glioma-associated oncogene 1 expression and its correlation with the expression of sonic hedgehog, E-cadherin and S100a4 in human hepatocellular carcinoma

Cited by 16 publications

References 12 publications

Histone acetyltransferase PCAF Up-regulated cell apoptosis in hepatocellular carcinoma via acetylating histone H4 and inactivating AKT signaling

Histone acetyltransferase PCAF Up-regulated cell apoptosis in hepatocellular carcinoma via acetylating histone H4 and inactivating AKT signaling

Caveolin-1 Is Up-Regulated by GLI1 and Contributes to GLI1-Driven EMT in Hepatocellular Carcinoma

Expression of glioma-associated oncogene 2 (Gli 2) is correlated with poor prognosis in patients with hepatocellular carcinoma undergoing hepatectomy

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