الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Background : Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. The mechanisms of initiation and development of liver neoplasms are still unclear. The human SET domain containing protein 1A (hSETD1A) gene belongs to the trithorax (TrxG) family of histone methyltransferases (HMT) that methylates lysine 4 at histone H3 tail. As known, alterations in histone modification can drive important cancerous processes such as proliferation, invasion, angiogenesis, and differentiation by perturbing normal gene expression patterns. hSETD1A has been shown to play a role in cell differentiation and tissue development, but very little is known about the role of hSETD1A in cancer, particularly in solid tumors. Objectives: The aim of the current study is to investigate the expression of hSETD1A gene as well as the target genes of Wnt signaling pathway (c-Myc and VEGFA) in patients with hepatocellular carcinoma.Methods: This study included 40 tissue samples were obtained from HCC patients. They were pathologically diagnosed to have liver cancer and subjected to surgical resection. In addition, 40 samples from the healthy safety margin of liver cancer of the same patients were included as a control group.The expression of hSETD1A gene and the target genes of Wnt signaling pathway (c-Myc and VEGFA) has been performed by quantitative real time RT-PCR as follow: 1) RNA extraction using Trizole reagent. 2) Reverse Transcription of RNA → cDNA. 3) Real Time PCR. Results: The results revealed that hSETD1A expression was increased in carcinoma tissue from HCC patients compared with adjacent normal tissue in these patients. On the other hand there was no statistically significant difference between cancerous and control samples as regard Wnt target genes (c-Myc and VEGFA).Conclusion: These data demonstrate that hSETD1A play a role in HCC. It may act through regulation of Wnt signaling pathway target genes or through other mechanism.