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目的:探讨奥沙利铂(oxaliplatin,L-OHP)对肝癌细胞HepG2增殖、黏附、迁移和侵袭等生物学行为的影响。方法:应用MTT法、Transwell、RT-PCR及Western印迹法检测L-OHP作用后,HepG 2细胞增殖、黏附、迁移、侵袭能力及RhoC mRNA和蛋白表达的变化。结果:L-OHP可显著抑制HepG 2细胞的增殖,同一时间不同浓度各组细胞的生长抑制率有明显差异(P<0.01),相同浓度下作用48和72 h组细胞的生长抑制率明显高于24 h组(P<0.01)。低毒剂量(2.5 mg/L)L-OHP作用HepG 2细胞30、60、90和120 min时,细胞的黏附能力明显降低(P<0.01),各时间点细胞的黏附抑制率分别为29.21%、27.27%、26.62%和24.76%。2.5 mg/L L-OHP作用HepG 2细胞24 h后,迁移和侵袭的细胞数明显减少(P<0.01),细胞的迁移和侵袭抑制率分别为53.68%和54.38%。2.5 mg/L L-OHP作用HepG2细胞4、6和8 d后,细胞RhoC mRNA和蛋白的表达水平逐渐下降(P<0.05)。结论:L-OHP能抑制肝癌细胞HepG 2的增殖,低毒剂量的L-OHP具有抑制肝癌细胞HepG 2黏附、迁移和侵袭的能力,其抗侵袭和转移的作用可能与下调细胞RhoC的表达有关。
Objective: To investigate the effects of oxaliplatin (L-OHP) on the biological behaviors of HepG2 cells such as proliferation, adhesion, migration and invasion. Methods: The proliferation, adhesion, migration, invasion and the expression of RhoC mRNA and protein in HepG2 cells were detected by MTT, Transwell, RT-PCR and Western blotting. Results: L-OHP significantly inhibited the proliferation of HepG 2 cells. The growth inhibition rates of different concentrations of L-OHP were significantly different at the same time (P <0.01). The growth inhibition rates of cells treated with same concentration for 48 and 72 h were significantly higher At 24 h (P <0.01). The cell adhesion capacity of HepG 2 cells was significantly decreased at low dose (2.5 mg / L) of L-OHP for 30, 60, 90 and 120 min (P <0.01), and the inhibition rates of cell adhesion were 29.21% , 27.27%, 26.62% and 24.76% respectively. After being treated with 2.5 mg / L L-OHP for 24 h, the number of migrated and infiltrated cells decreased significantly (P <0.01). The inhibitory rates of migration and invasion were 53.68% and 54.38%, respectively. After 4, 6 and 8 d of 2.5 mg / L L-OHP treatment, the expression of RhoC mRNA and protein in HepG2 cells gradually decreased (P <0.05). CONCLUSION: L-OHP can inhibit the proliferation of HepG2 cells. Low-dose L-OHP can inhibit the adhesion, migration and invasion of HepG2 cells. The anti-invasion and metastasis of L-OHP may be related to the down-regulation of RhoC expression .