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miR-455-5p在结直肠癌中的表达及生物学特性
引用本文:王金秋,鲁杨,柯孔亮,张乐鸣.miR-455-5p在结直肠癌中的表达及生物学特性[J].浙江医学,2018,40(8):796-802,812.
作者姓名:王金秋  鲁杨  柯孔亮  张乐鸣
作者单位:宁波大学医学院
摘    要:目的探讨miR-455-5p在结直肠癌(CRC)中的表达及生物学特性。方法收集40例CRC患者经手术切除的结肠和直肠癌组织标本及癌旁10cm的正常黏膜组织标本。采用qRT-PCR法检测CRC组织及癌旁正常黏膜组织中miR-455-5p的表达水平;采用脂质体转染试剂转染CRC细胞,Brdu增殖实验检测转染后CRC细胞增殖能力,流式细胞仪检测转染后CRC细胞凋亡率。应用生物信息学方法预测并验证miR-455-5p的靶基因。结果CRC组织miR-455-5p的相对表达量低于癌旁正常黏膜组织(P<0.01)。经转染后CRC细胞中,上调miR-455-5p可抑制CRC细胞增殖和迁移,促进细胞凋亡。数据库预测PIK3R1可能是miR-455-5p的靶基因,上调miR-455-5p可抑制PIK3R1mRNA及蛋白表达。结论miR-455-5p在CRC组织中呈低表达,其生物学特性是miR-455-5p具有抑制CRC细胞生长的作用,其机制可能与调控PIK3R1的表达有关。

关 键 词:结直肠癌  逆转录作用  靶基因  生物学特性

Expression of miR-455-5p in colorectal carcinoma and its relation to biological features of cancer
Abstract:Objective To investigate the expression of miR-455-5p in colorectal carcinoma and its relation to biological features of cancer. Methods The surgical specimens of cancer tissue and pericancerous mucosa tissue were collected from 40 cases of colorectal carcinoma. The expression of miR-455-5p was determined by qRT-PCR in the cancer tissue and pericancerous tissue. The colorectal cancer SW-480, HCT-116, HT-29 cells were transfected with miR-455-5p-mimic or inhibitor, respectively. The cell growth and proliferation capacity were assayed by Brdu method; the cell apoptosis was tested by flow cytometry; the target genes of miR-455-5p were predicted with bioinformatic analysis. Results The expression of miR-455-5p was down-regulation in colorectal cancer tissue compared with pericancerous tissue. In the colorectal cancer cells transfected with miR-455-5p-mimic, the expression of miR-455-5p was up-regulated, and the cell proliferation and migration were inhibited, and apoptosis was promoted. Bioinformatic analysis showed that PIK3R1 might be the target gene of miR-455-5p. The up-regulation of miR-455-5p inhibited the expression of PIK3R1 mRNA and protein. Conclusion The expression of miR-455-5p is down-regulated in colorectal cancer, indicating that miR-455-5p may inhibit the growth of CRC cells, which may be related to the regulation of PIK3R1 expression.
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