Down-regulation of LINC00667 hinders renal tubular epithelial cell apoptosis and fibrosis through miR-34c

被引：10
作者：
Huang, P. [1 ]
Gu, X. -J. [1 ]
Huang, M. -Y. [1 ]
Tan, J. -H. [1 ]
Wang, J. [1 ]
机构：
[1] Youjiang Med Univ Nationalities, Dept Nephrol, Affiliated Hosp, 18th Zhongshan 2nd Rd, Baise 533000, Guangxi, Peoples R China
来源：
CLINICAL & TRANSLATIONAL ONCOLOGY | 2021年 / 23卷 / 03期
关键词：
LINC00667; miR-34c; Chronic renal disease; Renal tubular epithelial cells; Apoptosis; Fibrosis; EXPRESSION; SIGNAL;
D O I：
10.1007/s12094-020-02451-2
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
Purpose This study aimed to down-regulate LINC00667 and inhibit apoptosis and fibrosis of renal tubular epithelial cells through miR-34c. Methods Altogether, 98 patients with chronic kidney disease treated in our hospital were selected as the study group, and 67 normal people were selected as the control group. Epithelial cells of proximal convoluted tubules in human renal cortex were purchased. TGF-beta 1 was used to induce fibrosis of HK-2 renal tubular epithelial cells. The expression of LINC00667, miR-34c, type I collagen (Col 1) and type III collagen (Col 3) were detected by qRT-PCR and WB. Results LINC00667 was highly expressed in cancer tissues and HK-2, while miR-34c was poorly expressed. Inhibition of LINC00667 and over-expression of miR-34c could inhibit the proliferation and invasion of chronic kidney disease cells, but increase the apoptosis rate. Down-regulation of LINC00667 could significantly reduce of Col 1 and Col 3 in renal interstitial fibroblasts induced by TGF-beta 1, while up-regulation of miR-34c could also achieve this effect. Double luciferase report confirmed that there was a targeted regulatory relationship between LINC00667 and miR-34c. Conclusion LINC00667 could reduce the proliferation and invasion of chronic kidney disease cells, increase the apoptosis rate by regulating miR-34c, and improve renal fibrosis.
引用
收藏
页码：572 / 581
页数：10
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