| Literature DB >> 33368623 |
Yeye Chen1,2, Xiaoyun Zhou1,2, Cheng Huang1,2, Li Li1,2, Yingzhi Qin1,2, Zhenhuan Tian1,2, Jia He1,2, Hongsheng Liu1,2.
Abstract
It has been demonstrated in previous studies that lncPART1 is dysregulated in non-small cell lung cancer (NSCLC). However, the function of lncPART1 in NSCLC is unclear. Therefore, this experimental design was based on LncPART1 to explore the pathogenesis of NSCLC. Real-time polymerase chain reaction was used to detect the expression of lncPART1 and miR-17-5p in NSCLC. Cell Counting Kit -8, colony formation, and transwell assays were used to examine the effects of lncPART1 and miR-17-5p on NSCLC cell proliferation and migration invasiveness. Target gene prediction, luciferase reporter assays were used to validate downstream target genes for lncPART1 and miR-17-5p. Western blot analysis was used to detect the expression of TGFBETAR2. LncPART1 was highly expressed in NSCLC. LncPART1 significantly promoted cell proliferation of NSCLC cells. miR-17-5p was down-expressed in NSCLC. miR-17-5p overexpression inhibited cell proliferation and migration invasion in NSCLC cells. LncPART1 was able to inhibit miR-17-5p expression and upregulate the expression level of TGFBETAR2. The results of in vivo animal models confirmed that lncPART1 promoted NSCLC progression by miR-17-5p/TGFBETAR2 axis. LncPART1 promoted the progression of NSCLC by miR-17-5p/TGFBETAR2 axis.Entities:
Keywords: LncRNAPART1; TGFBETAR2; miR-17-5p; non-small cell lung cancer; proliferation
Year: 2020 PMID: 33368623 DOI: 10.1002/jcb.29714
Source DB: PubMed Journal: J Cell Biochem ISSN: 0730-2312 Impact factor: 4.429