Immunohistochemical analysis of p53, cyclinD1, RB1, c-fos and N-ras gene expression in hepatocellular carcinoma in Iran

Moghaddam, Seyed Javad; Haghighi, Ehsan Nobakht; Samiee, Shahram; Shahid, Negin; Keramati, A. R.; Dadgar, Sina; Zali, Mohammad Reza

doi:10.3748/wjg.v13.i4.588

Cited by 26 publications

(19 citation statements)

References 30 publications

(36 reference statements)

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“…Cyclin D1 is a protein closely associated with cell proliferation, and it is mainly involved in the G1 phase of the cell cycle. It plays an extremely important role in the regulation of the cell cycle (Moghaddam et al, 2007). Our results suggested that dexamethasone significantly reduced PCNA and cyclin D1 expression, and with the reduction in cyclin D1 expression, mitotic complexes were not formed.…”

Section: Discussionmentioning

confidence: 67%

Inhibitory effect of dexamethasone on Lewis mice lung cancer cells

Geng¹,

Wang²,

Jing³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Recent studies have found that glucocorticoids are closely associated with oncogenesis and the development of many types of tumors. The aim of this study was to observe the effect of dexamethasone on the growth and angiogenesis of transplanted Lewis lung carcinoma in mice. Lewis lung carcinoma cells were inoculated subcutaneously into the right axilla of C57BL/6 mice, and the mice were randomly divided into 3 groups: the control group, cisplatin group, and dexamethasone group. From day 7 after inoculation, all the mice were given different treatments for 10 days, and changes in xenograft tumor volumes were monitored. All mice were sacrificed on day 17, and the tumors were obtained and weighed and the tumor inhibitory rate was calculated. The expression levels of hypoxia inducible factor 1α (HIF-1α) and vascular endothelial growth factor (VEGF), as well as the microvessel density (MVD) in the tumor mass, were measured by immunohistochemistry. Tumor growth was suppressed in the cisplatin group and dexamethasone group. The weights of tumors were markedly decreased in the cisplatin group and dexamethasone group compared with the control group (P < 0.05). The expression levels of HIF-1α and VEGF and the MVD were significantly lower in the cisplatin group and dexamethasone group than in the control group (P < 0.05). However, these levels were not significantly different between the cisplatin group and dexamethasone group (P > 0.05). Dexamethasone can effectively inhibit the growth and angiogenesis of Lewis lung carcinoma by inhibiting the expression of HIF-1α and VEGF.

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Section: Discussionmentioning

confidence: 67%

Inhibitory effect of dexamethasone on Lewis mice lung cancer cells

Geng¹,

Wang²,

Jing³

et al. 2014

Genet. Mol. Res.

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“…One study using immunohistochemical analysis demonstrated that c-FOS serves a key role in HCC pathogenesis (32). The upregulation of c-FOS and Jun proto-oncogene mediated by protein kinase R promotes HCC proliferation (33).…”

Section: Discussionmentioning

confidence: 99%

Analysis of expression profile data identifies key genes and pathways in hepatocellular carcinoma

Jiang¹,

Hao²

2017

Oncol Lett

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Abstract. The aims of the present study were to identify key genes and pathways associated with hepatocellular carcinoma (HCC) progression and predict compounds potentially associated with this type of carcinogenesis. The gene expression profile data of the GSE49515 dataset was obtained from the Gene Expression Omnibus database. The limma software package was used to identify the differentially expressed genes (DEGs). Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the Biological Networks Gene Ontology tool and the Database for Annotation, Visualization and Integrated Discovery, respectively. The Michigan Molecular Interactions database plugin within the Cytoscape software platform was used to perform protein-protein interaction (PPI) network analysis. Chemical-gene interaction data for HCC were obtained from the Comparative Toxicogenomics Database to evaluate the associations between drugs and specific genes. A total of 302 DEGs, including 231 downregulated and 71 upregulated, were identified. Cytokine-cytokine receptor interaction and chemokine signaling were the significantly enriched pathways. Additionally, PPI network analysis indicated a total of 13 highest degree hub nodes, including FBJ murine osteosarcoma viral oncogene homolog (FOS) and DNA damage-inducible transcript 3 protein (DDIT3). Chemical-gene interaction analysis revealed that FUN and FOS were targeted by >500 compounds, while >200 genes were targeted by 2,3,7,8-tetrachlorodibenzodioxin and benzo(α)pyrene. In conclusion, the present study demonstrated that FOS, DDIT3, the cytokine-cytokine receptor interaction pathway and the chemokine signaling pathway may be key genes and pathways associated with the development of HCC. Furthermore, exposure to 2,3,7,8-tetrachlorodibenzodioxin or benzo(α)pyrene may lead to hepatocarcinogenesis.

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“…Upregulated expression of EGF-R is a frequent finding in HCC [37][38][39] , and increased EGF-R signaling has been associated with a poorer prognosis [40] . c-Fos is also frequently overexpressed in HCC tumoral tissues [13][14][15]41] . Our data, therefore, suggest that a causal relationship could exist between c-Fos and EGF-R overexpression in HCC.…”

Section: Discussionmentioning

confidence: 99%

c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1

Güller¹,

Toualbi-Abed²,

Legrand³

et al. 2008

WJG

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flow cytometry showed that c-Fos accelerated the cell cycle kinetics. Following serum stimulation, Cyclin D1 was more abundantly expressed in c-Fos overexpressing cells. Cyclin D1 accumulation did not result from increased transcriptional activation, but from nuclear stabilization. Overexpression of c-Fos correlated with higher nuclear levels of inactive phosphorylated GSK-3β, a kinase involved in Cyclin D1 degradation and higher levels of EGF-R mRNA, and EGF-R protein compared to IHH-C both in serum starved, and in serum stimulated cells. Abrogation of EGF-R signalling in IHHFos by treatment with AG1478, a specific EGF-R tyrosine kinase inhibitor, prevented the phosphorylation of GSK-3β induced by serum stimulation and decreased Cyclin D1 stability in the nucleus. METHODS:IHHs stably transfected with c-Fos (IHHFos) or an empty vector (IHH-C) were grown in medium supplemented with 1% serum or stimulated with 10% serum. Cell proliferation was assessed by cell counts, 3H-thymidine uptake and flow cytometry analyses. The levels of cell cycle regulatory proteins (Cyclin D1, E, A) cyclin dependent kinases (cdk) cdk2, cdk4, cdk6, and their inhibitors p15, p16, p21, p27, total and phosphorylated GSK-3β and epidermal growth factor receptor (EGF-R) were assayed by Western blotting. Analysis of Cyclin D1 mRNA levels was performed by reverse transcription-polymerase chain reaction and real-time polymerase chain reaction (PCR) analysis. Stability of Cyclin D1 was studied by cycloheximide blockade experiments. RESULTS: Stable c-Fos overexpression increased cell proliferation under low serum conditions and resulted in a two-fold increase in [3 H]-thymidine incorporation following serum addition. Cell cycle analysis by

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Immunohistochemical analysis of p53, cyclinD1, RB1, c-fos and N-ras gene expression in hepatocellular carcinoma in Iran

Cited by 26 publications

References 30 publications

Inhibitory effect of dexamethasone on Lewis mice lung cancer cells

Inhibitory effect of dexamethasone on Lewis mice lung cancer cells

Analysis of expression profile data identifies key genes and pathways in hepatocellular carcinoma

c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1

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