LncRNA PART1 promotes cell proliferation and progression in non‐small‐cell lung cancer cells via sponging miR‐17‐5p

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. 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.