Purpose: This study aims to explore the differential expression of SFN gene and its regulatory role in different hepatocarcinoma cells, and the impact on hepatocarcinoma. Materials and Methods: High and low SFN expression cells were screened by qRT-PCR and western blotting methods. SFN over expression and interference vectors were constructed. Cell viability was detected by CCK8 kit, cell cycle and apoptosis were detected by flow cytometry. Cell invasion and migration were detected. CCNB1 and CDK1 expression levels were detected by qRT-PCR and Western blotting methods. Results: The high SFN expression BEL7402 cells and the low SFN expression Hep3B cells were screened from Hep3B, HepG2, and BEL7402 cells. The activity of Hep3B cells overexpression vector SFN-pcDNA3.1(+) decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of S phase increased. The activity of BEL7402 cells transfected with SFN siRNA decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of G2/M increased. Interference and overexpression vectors have little effect on the invasion and migration of the two cells. The expression of CDK1 in Hep3B cells decreased significantly, the expression of CDK1 and CCNB1 in BEL7402 cells increased significantly. Conclusions: The differentially expressed SFN gene can regulate the growth of the two hepatocarcinoma cells, high expression of SFN gene can inhibit their growth. The mechanism may be achieved by regulating CCNB1 and CDK1 expression.

目的：本研究旨在探讨SFN基因在不同肝癌细胞中的差异表达及其调控作用，以及对肝癌的影响。材料和方法：通过qRT-PCR和蛋白质印迹方法筛选高和低SFN表达细胞。构建了SFN过表达和干扰载体。CCK8试剂盒检测细胞活力，流式细胞仪检测细胞周期和细胞凋亡。检测细胞侵袭和迁移。CCNB1 和 CDK1 表达水平通过 qRT-PCR 和蛋白质印迹方法检测。结果：从Hep3B、HepG2和BEL7402细胞中筛选出SFN高表达BEL7402细胞和SFN低表达Hep3B细胞。Hep3B细胞过表达载体SFN-pcDNA3.1(+)活性降低，细胞凋亡增加，G0/G1 比值降低，S 相比值增加。SFN siRNA转染BEL7402细胞活性降低，细胞凋亡增加，G0/G1比值降低，G2/M比值升高。干扰和过表达载体对两种细胞的侵袭和迁移影响不大。Hep3B细胞中CDK1的表达显着降低，BEL7402细胞中CDK1和CCNB1的表达显着增加。结论：差异表达的SFN基因可调节两种肝癌细胞的生长，SFN基因的高表达可抑制其生长。该机制可能是通过调节 CCNB1 和 CDK1 的表达来实现的。G0/G1比值下降，G2/M比值增加。干扰和过表达载体对两种细胞的侵袭和迁移影响不大。Hep3B细胞中CDK1的表达显着降低，BEL7402细胞中CDK1和CCNB1的表达显着增加。结论：差异表达的SFN基因可调节两种肝癌细胞的生长，SFN基因的高表达可抑制其生长。该机制可能是通过调节 CCNB1 和 CDK1 的表达来实现的。G0/G1比值下降，G2/M比值增加。干扰和过表达载体对两种细胞的侵袭和迁移影响不大。Hep3B细胞中CDK1的表达显着降低，BEL7402细胞中CDK1和CCNB1的表达显着增加。结论：差异表达的SFN基因可调节两种肝癌细胞的生长，SFN基因的高表达可抑制其生长。该机制可能是通过调节 CCNB1 和 CDK1 的表达来实现的。差异表达的SFN基因可以调节两种肝癌细胞的生长，SFN基因的高表达可以抑制它们的生长。该机制可能是通过调节 CCNB1 和 CDK1 的表达来实现的。差异表达的SFN基因可以调节两种肝癌细胞的生长，SFN基因的高表达可以抑制它们的生长。该机制可能是通过调节 CCNB1 和 CDK1 的表达来实现的。