Construction of microRNA-144 plasmid and its effect on biological behavior of human hepatocellular carcinoma | miR-144表达质粒的构建及其对肝癌细胞生物学行为的影响
2011
Wang Zheng, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an (China) | Zhang Mingxin, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an (China) | Zhang Lingmin, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an (China)
Chinese. 构建microRNA-144（miR-144）的真核表达质粒，并探讨miR-144对人肝癌细胞株HepG2生物学行为的影响，为肝癌的生物学治疗提供依据。构建miR-144真核表达质粒并合成miR-144反义寡核苷酸，通过实时定量PCR检测miR-144的表达，采用MTT比色法及流式细胞仪技术，检测抑制与过表达miR-144对肝癌细胞增殖、凋亡和细胞周期的影响。成功构建了miR-144的真核表达质粒，过表达miR-144能够显著抑制肝癌细胞的增殖（P0.05），促进细胞凋亡（P0.05）；而抑制miR-144的表达则得到相反的结果；抑制与过表达miR-144对肝癌细胞周期的影响都不大（P0.05）。miR-144能影响人肝癌细胞株HepG2的生物学行为，具有抑制肝癌细胞增殖的作用。
Show more [+] Less [-]English. The study was to construct microRNA-144 (miR-144) eukaryotic expression vector and to detect the effect of miR-144 on the proliferation, apoptosis, migration, and invasion of human hepatocellular carcinoma HepG2 cells. After the construction of miR-144 expression plasmid and miR-144 antisense oligonucleotides, the effect of them on expression of miR-144 was confirmed by real-time PCR. The proliferation, apoptosis, migration, and invasion of HepG2 were detected by MTT assay and flow cytometry respectively. Overexpression of miR-144 could significantly inhibit the proliferation (P0.05) and promote the apoptosis of HepG2 (P0.05). However, inhibition of miR-144 provides the opposite results. However, alteration of miR-144 could not influence the cell cycle (P0.05). miR-144 could influence the biological behavior of primary liver cancer cell HepG2 and acts as a tumor suppressor.
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