Yongjie Huang1, Ran Ni2, Jing Wang3, Ying Liu4. 1. Department of Senile Respiratory and Sleep, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. 2. Department Two of Respiratory Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. 3. Department Two of Respiratory Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China. Electronic address: wjgoodok5252@sohu.com. 4. Department Five of Respiratory Medicine, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Abstract
BACKGROUND: Long non-coding RNA (lncRNA) distal-less homeobox 6 antisense 1 (DLX6-AS1) was reported to be dysregulated in lung cancer. However, detailed roles of DLX6-AS1 in the pathogenesis of non-small cell lung cancer (NSCLC) were largely unknown. METHODS: The expression of DLX6-AS1 was measured in NSCLC tissues and cells by quantitative real-time PCR (qRT-PCR). The abundance of proline rich 11 (PRR11) were detected by qRT-PCR and western blot, respectively. The effects of DLX6-AS1 and PRR11 on cell proliferation, migration, invasion and apoptosis were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell and flow cytometry analysis, respectively. Luciferase reporter assay, qRT-PCR and western blot were performed to confirm the interaction between miR-144 and DLX6-AS1 or PRR11. Tumor xenograft assay was performed to verify the role of DLX6-AS1 in NSCLC in vivo. RESULTS: DLX6-AS1 and PRR11 were elevated in NSCLC tissues and cells. DLX6-AS1 was positively correlated with PRR11 mRNA expression in NSCLC tissues. Knockdown of DLX6-AS1 and PRR11 significantly suppressed cell proliferation, migration and invasion and induced apoptosis in NSCLC cells, which was reversed by PRR11 overexpression. In addition, DLX6-AS1 and PRR11 were demonstrated to interact with microRNA-144 (miR-144) and DLX6-AS1 upregulated PRR11 expression by acting as a competing endogenous RNA (ceRNA) of miR-144 in NSCLC cells. Furthermore, DLX6-AS1 knockdown suppressed tumor growth in NSCLC in vivo by upregulating miR-144 and downregulating PRR11. CONCLUSION: Knockdown of DLX6-AS1 inhibited cell proliferation, migration, invasion and promoted apoptosis by downregulating PRR11 expression and upregulating miR-144 in NSCLC.
BACKGROUND: Long non-coding RNA (lncRNA) distal-less homeobox 6 antisense 1 (DLX6-AS1) was reported to be dysregulated in lung cancer. However, detailed roles of DLX6-AS1 in the pathogenesis of non-small cell lung cancer (NSCLC) were largely unknown. METHODS: The expression of DLX6-AS1 was measured in NSCLC tissues and cells by quantitative real-time PCR (qRT-PCR). The abundance of proline rich 11 (PRR11) were detected by qRT-PCR and western blot, respectively. The effects of DLX6-AS1 and PRR11 on cell proliferation, migration, invasion and apoptosis were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell and flow cytometry analysis, respectively. Luciferase reporter assay, qRT-PCR and western blot were performed to confirm the interaction between miR-144 and DLX6-AS1 or PRR11. Tumor xenograft assay was performed to verify the role of DLX6-AS1 in NSCLC in vivo. RESULTS:DLX6-AS1 and PRR11 were elevated in NSCLC tissues and cells. DLX6-AS1 was positively correlated with PRR11 mRNA expression in NSCLC tissues. Knockdown of DLX6-AS1 and PRR11 significantly suppressed cell proliferation, migration and invasion and induced apoptosis in NSCLC cells, which was reversed by PRR11 overexpression. In addition, DLX6-AS1 and PRR11 were demonstrated to interact with microRNA-144 (miR-144) and DLX6-AS1 upregulated PRR11 expression by acting as a competing endogenous RNA (ceRNA) of miR-144 in NSCLC cells. Furthermore, DLX6-AS1 knockdown suppressed tumor growth in NSCLC in vivo by upregulating miR-144 and downregulating PRR11. CONCLUSION: Knockdown of DLX6-AS1 inhibited cell proliferation, migration, invasion and promoted apoptosis by downregulating PRR11 expression and upregulating miR-144 in NSCLC.