机构地区:[1]四川省绵竹市人民医院,四川绵竹618200 [2]中国人民解放军西部战区总医院药剂科,四川成都610083
出 处:《河北医学》2023年第1期70-75,共6页Hebei Medicine
基 金:2019四川省医学会静脉栓塞栓塞症防治(恒瑞)专项科研课题,(编号:2019HR02)。
摘 要:目的:探究氟伐他汀钠对结直肠癌SW620细胞增殖、凋亡的影响及可能机制。方法:体外培养SW620细胞、正常结直肠上皮FHC细胞,qRT-PCR法检测细胞中lncRNA PTPRG-AS1表达。SW620细胞分为对照组、氟伐他汀钠-低、中、高组、si-PTPRG-AS1组、si-NC组、氟伐他汀钠+pcDNA-PTPRG-AS1组、氟伐他汀钠+pcDNA组。CCK-8法、克隆形成实验、流式细胞术分别检测细胞活性、克隆形成数、凋亡率,Western blot法检测凋亡相关蛋白(cleaved-caspase3、cleaved-caspase9)表达。结果:结直肠癌SW620细胞中lncRNA PTPRG-AS1表达量高于FHC细胞(4.38±0.31 vs 1.00±0.00,P<0.05);氟伐他汀钠-低、中、高组细胞活性、克隆形成数均低于对照组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均高于对照组(P<0.05),且lncRNA PTPRG-AS1表达量低于对照组(P<0.05);si-PTPRG-AS1组细胞活性、克隆形成数均低于si-NC组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均高于si-NC组(P<0.05);氟伐他汀钠+pcDNA-PTPRG-AS1组细胞活性、克隆形成数均高于氟伐他汀钠+pcDNA组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均低于氟伐他汀钠+pcDNA组(P<0.05)。结论:氟伐他汀钠可能通过下调lncRNA PTPRG-AS1表达抑制结直肠癌SW620细胞增殖,并促进其凋亡。Objective:To explore the effect and possible mechanism of fluvastatin sodium on the proliferation and apoptosis of colorectal cancer SW620 cells.Methods:SW620 cells and normal colorectal epithelial FHC cells were cultured in vitro,and the expression of lncRNA PTPRG-AS1 in the cells was detected by qRT-PCR.SW620 cells were divided into control group,fluvastatin sodium-low,medium and high groups,si-PTPRG-AS1 group,si-NC group,fluvastatin sodium+pcDNA-PTPRG-AS1 group,fluvastatin sodium+pcDNA group.CCK-8 method,clone formation assay and flow cytometry were used to detect cell viability,clone formation number,apoptosis rate,and Western blot was used to detect the expression of apoptosis-related proteins(cleaved-caspase3,cleaved-caspase9).Results:The expression of lncRNA PTPRG-AS1 in colorectal cancer SW620 cells was higher than that in FHC cells(4.38±0.31 vs 1.00±0.00,P<0.05).The cell viability and the number of colonies formed in the fluvastatin sodium-low,medium and high groups were lower than those in the control group(P<0.05),but the apoptosis rate and protein(cleaved-caspase3,cleaved-caspase9)expression were higher than those in the control group(P<0.05),and the expression of lncRNA PTPRG-AS1 was lower than that of the control group(P<0.05).The cell viability and the number of colonies formed in the si-PTPRG-AS1 group were lower than those in the si-NC group(P<0.05),but the apoptosis rate and protein(cleaved-caspase3,cleaved-caspase9)expression were higher than those in the si-NC group(P<0.05).The cell viability and the number of colonies formed in the fluvastatin sodium+pcDNA-PTPRG-AS1 group were higher than those in the fluvastatin sodium+pcDNA group(P<0.05),but the apoptosis rate and protein(cleaved-caspase3,cleaved-caspase9)expression were lower than those in the fluvastatin sodium+pcDNA group(P<0.05).Conclusion:Fluvastatin sodium may inhibit the proliferation and promote apoptosis of colorectal cancer SW620 cells by down-regulating the expression of lncRNA PTPRG-AS1.
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