目的:探讨小干扰RNA降低组织蛋白酶B(Cat B)基因表达对HepG2细胞增殖、运动及侵袭能力的影响。方法:将肝癌HepG2细胞分为Cat B siRNA干扰组、阴性对照siRNA干扰组(阴性对照组)、空脂质体组和空白对照组。脂质体转染法将Cat B siRNA转染入HepG2细胞;半定量RT-PCR和蛋白质印迹法检测转染后48hCat B的表达变化;收集转染后48h的细胞,再分别以CCK-8法、划痕实验和Transwell侵袭实验检测各组细胞增殖、运动及侵袭能力的变化。结果:半定量RT-PCR和蛋白质印迹法检测Cat B mRNA和蛋白水平表达变化,Cat B siRNA干扰组较其余各组均明显降低,差异有统计学意义,P<0.05。CCK-8法测细胞生长曲线示,将转染后48h的细胞种入96孔板后12h,Cat B siRNA干扰组增殖能力较对照组明显降低,差异有统计学意义,P<0.05。划痕实验中,Cat B siRNA干扰组细胞迁移距离较对照组明显降低,差异有统计学意义,P<0.05。Transwell侵袭实验中,Cat B siRNA干扰组穿膜细胞数较对照组明显降低,差异有统计学意义,P<0.05。结论:特异性干扰Cat B基因表达可抑制HepG2细胞的增殖、运动及侵袭能力。
肝癌是全球癌症相关死亡的第三大原因,存在早期诊断困难、治疗选择受限及复发率高的问题。因此,深入研究肝癌的分子机制,发现新的治疗靶点和方法,对改善肝癌诊断和预后具有重要意义。Tribbles假激酶(TRIB1、TRIB2、TRIB3)因其在调节炎症、代谢和癌症中的独特作用已经成为研究热点。它们通过调控细胞周期在肝癌中起关键作用,并可能影响治疗抵抗性和免疫逃逸机制。文章总结近年来Tribbles假激酶家族在肝癌中作用机制的研究进展,旨在为肝癌的诊断、治疗和预后提供新的思路和策略。Liver cancer is the third leading cause of cancer-related deaths globally, characterized by difficulties in early diagnosis, limited treatment options, and high recurrence rates. Therefore, in-depth research on the molecular mechanisms of liver cancer to discover new therapeutic targets and methods is crucial for improving liver cancer diagnosis and prognosis. Tribbles pseudokinases (TRIB1, TRIB2, TRIB3) have become research hotspots due to their unique roles in regulating inflammation, metabolism, and cancer. They play a key role in liver cancer by regulating the cell cycle and may also influence treatment resistance and immune evasion mechanisms. This paper summarizes recent research progress on the mechanisms of the Tribbles pseudokinase family in liver cancer, aiming to provide new ideas and strategies for liver cancer diagnosis, treatment, and prognosis.
