a College of Clinical Medicine , Ningxia Medical University , Yinchuan , P.R. China.
b Ningxia Institute For Human Stem Cell Research , General Hospital of Ningxia Medical University , Yinchuan , P.R. China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):1200-1206. doi: 10.1080/21691401.2019.1593998.
To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism.
LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS + miR-NC group (transfected negative control samples), LPS + miR-16-5p group (transfected miR-16-5p mimics); LPS + si-NC group (transfected negative control samples), LPS + si-CXCR3 group (transfected si-CXCR3); LPS + miR-16-5p + pcDNA3.1 group (co-transfected miR-16-5p mimics and pcDNA3.1), LPS + miR-16-5p + pcDNA3.1-CXCR3 group (co-transfected miR-16-5p mimics and pcDNA3.1-CXCR3) were transfected into A549 cells by liposome method. Western blot was used to detect protein expression of CXCR3, IL-6 and TNF-α in A549 cells; apoptosis of A549 cells was detected by flow cytometry.
Compared with the control group, the expression of miR-16-5p mRNA was significantly decreased in A549 cells in LPS group, and the mRNA and protein expression of CXCR3 were significantly increased (p < .05). Overexpression of miR-16-5p and knockdown of CXCR3 both can down-regulated protein expression of IL-6 and TNF-α, and up-regulated apoptosis in LPS-induced A549 cell; CXCR3 is a target of miR-16-5p. Overexpression of CXCR3 rescued the protective effect of miR-16-5p on LPS-induced A549 cell injury.
miR-16-5p can protect LPS-induced A549 cell injury, and its mechanism may be related to the targeted regulation of CXCR3, which could provide a new target for targeted therapy of lung cancer.
研究 miR-16-5p 对肺癌细胞损伤和凋亡的影响及其机制。
用 LPS 诱导肺癌细胞 A549 损伤；qRT-PCR 法检测 A549 细胞中 miR-16-5p 和 CXCR3 的表达。设 Con（无 LPS 处理）组、LPS+miR-NC 组（转染阴性对照样本）、LPS+miR-16-5p 组（转染 miR-16-5p 模拟物）；LPS+si-NC 组（转染阴性对照样本）、LPS+si-CXCR3 组（转染 si-CXCR3）；LPS+miR-16-5p+pcDNA3.1 组（共转染 miR-16-5p 模拟物和 pcDNA3.1）、LPS+miR-16-5p+pcDNA3.1-CXCR3 组（共转染 miR-16-5p 模拟物和 pcDNA3.1-CXCR3）。用脂质体法将 LPS+miR-16-5p+pcDNA3.1 组、LPS+miR-16-5p+pcDNA3.1-CXCR3 组分别转染 A549 细胞。Western blot 法检测 A549 细胞中 CXCR3、IL-6 和 TNF-α 的蛋白表达；流式细胞术检测 A549 细胞凋亡。
与对照组相比，LPS 组 A549 细胞中 miR-16-5p mRNA 的表达明显降低，而 CXCR3 的 mRNA 和蛋白表达明显增加（p＜0.05）。过表达 miR-16-5p 和敲低 CXCR3 均能下调 LPS 诱导的 A549 细胞中 IL-6 和 TNF-α 的蛋白表达，并上调细胞凋亡；CXCR3 是 miR-16-5p 的靶基因。过表达 CXCR3 可挽救 miR-16-5p 对 LPS 诱导的 A549 细胞损伤的保护作用。
miR-16-5p 可保护 LPS 诱导的 A549 细胞损伤，其机制可能与靶向调节 CXCR3 有关，为肺癌的靶向治疗提供了新的靶点。
