氟伐他汀钠通过下调lncRNA PTPRG-AS1表达对结直肠癌SW620细胞增殖凋亡的影响

doi:10.3969/j.issn.1006-6233.2023.01.013

摘要
图/表
参考文献
相关文章 (15)

全文: PDF (1759 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

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。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章

关键词 ：结直肠癌, 氟伐他汀钠, lncRNA PTPRG-AS1, 细胞增殖, 凋亡

Abstract：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.

Key words： Colorectal cancer Fluvastatin sodium LncRNA PTPRG-AS1 Cell proliferation Apoptosis

基金资助: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)

引用本文:

刘芝, 董丽娥, 陈斌, 陈子鑫. 氟伐他汀钠通过下调lncRNA PTPRG-AS1表达对结直肠癌SW620细胞增殖凋亡的影响[J]. 河北医学, 2023, 29(1): 70-75.
LIU Zhi, et al. Effects of Fluvastatin Sodium on the Proliferation and Apoptosis of Colorectal Cancer SW620 Cells by Down-Regulating the Expression of LncRNA PTPRG-AS1. HeBei Med, 2023, 29(1): 70-75.

链接本文:

http://www.hbyxzzs.cn/CN/10.3969/j.issn.1006-6233.2023.01.013 或 http://www.hbyxzzs.cn/CN/Y2023/V29/I1/70

[1] 中华人民共和国国家卫生健康委员会.中国结直肠癌诊疗规范(2020年版)[J].中华外科杂志,2020,58(8):561-585.
[2] Blondy S,David V,Verdier M,et al.5-Fluorouracil resistance mechanisms in colorectal cancer:from classical pathways to promising processes[J].Cancer Sci,2020,111(9):3142-3154.
[3] Ishikawa S,Hayashi H,Kinoshita K,et al.Statins inhibit tumor progression via an enhancer of zeste homolog 2-mediated epigenetic alteration in colorectal cancer[J].Int Cancer,2014,135(11):2528-2536.
[4] Wu K M,Wang Z,Huang Y L,et al.LncRNA PTPRG-AS1 facilitates glycolysis and stemness properties of esophageal squamous cell carcinoma cells through miR-599/PDK1 axis[J].Gastroenterol Hepatol,2022,37(3):507-517.
[5] Shi J J,Xu X J,Zhang D,et al.Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression[J].Ovarian Res,2020,13(1):127-140.
[6] 李敬霞,刘艳.lncRNA PTPRG-AS1通过靶向miR-124-3p调控肝癌细胞凋亡和放射敏感性的研究机制[J].现代肿瘤医学,2021,29(10):1676-1682.
[7] 刘鸿雁,孙冲,李倩,等.氟伐他汀钠对皮肤鳞状细胞癌细胞增殖、凋亡及PI3K/AKT/mTOR通路的影响[J].中国医科大学学报,2020,49(9):841-845.
[8] Alhakamy N A,Ahmed O A A,Md S,et al.Mastoparan,a peptide toxin from wasp venom conjugated fluvastatin nanocomplex for suppression of lung cancer cell growth[J].Polymers (Basel),2021,13(23):4225-4238.
[9] Mohapatra D,Das B,Suresh V,et al.Fluvastatin sensitizes pancreatic cancer cells toward radiation therapy and suppresses radiation- and/or TGF-β-induced tumor-associated fibrosis[J].Lab Invest,2022,102(3):298-311.
[10] Cai Y,Zhao F.Fluvastatin suppresses the proliferation,invasion,and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6)[J].Bioengineered,2021,12(2):12509-12520.
[11] Zhang Y,Peng C F,Li J,et al.Long non-coding RNA CCDC144NL-AS1 promotes cell proliferation by regulating the miR-363-3p/GALNT7 axis in colorectal cancer[J].Cancer,2022,13(3):752-763.
[12] Jiang Y,Yu X Y,Sun H X,et al.Long non-coding RNA HOXA-AS3 facilitates the malignancy in colorectal cancer by miR-4319/SPNS2 axis[J].Physiol Biochem,2021,77(4):653-666.
[13] Ge R L,Yang P,Wen B T.Upregulation of long-noncoding RNA PTPRG-AS1 can predict the poor prognosis and promote migration and invasion in patients with osteosarcoma[J].Oncol Lett,2021,21(6):464-471.
[14] Yi L,Ouyang L,Wang S,et al.Long noncoding RNA PTPRG-AS1 acts as a microRNA-194-3p sponge to regulate radiosensitivity and metastasis of nasopharyngeal carcinoma cells via PRC1[J].Cell Physiol,2019,234(10):19088-19102.