关键词: 肝癌, cyclinD1, ERK, NF-KB, miRNA-5102

Abstract: Abstract: Objective To investigate the regulatory mechanisms contributing to over-expressed cyclinD1 in Hras12V induced hepatocellular carcinoma． Method The liver tumor tissues and peri-tumor tissues of 9-month-old male H-ras12V transgenic mice and normal liver tissues of male C57BL /6J mice were sampled． Part of each sample was fixed in 10% formalin and undergone paraffin-embedded tissue section，HE staining，and pathological analysis． Part of each sample was frozen in liquid nitrogen for extraction of total RNA and protein． miRNA expression was analyzed by High-Throughput Sequencing． The cyclin D1 and miR-5102 gene expression were examined by qRT-PCR． The protein levels of cyclin D1，p-ERK，ERK，and IκB were detected by Western blot． Result Compared with the normal liver tissues and peri-tumor tissues，the mRNA and protein expression levels of cyclin D1 in tumor tissues was significantly increased ( P ＜ 0. 05) ; The protein and phosphorylation levels of signaling molecule ERK were significantly increased; And the protein level of inhibitor IκB were significantly reduced． The expression level of miR-5102 did not change significantly among the three sample groups． Conclusion In the process of H-ras12V-induced liver tumorigenesis，activation of MAPK /ERK and NF-κB signaling pathways contribute to the over-expression of cyclin D1．

Key words: hepatocellular carcinoma, cyclinD1, ERK, NF-κB, miRNA-5102