Long non-coding RNA DLX6-AS1 knockdown suppresses the tumorigenesis and progression of non-small cell lung cancer through microRNA-16-5p/BMI1 axis
| Autor: | Chengde Wu, Fangyong Fu, Wei Lin |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cancer Research
Gene knockdown microRNA-16-5p (miR-16-5p) DLX6 Long non-coding RNA distal-less homeobox 6 antisense RNA 1 (lncRNA DLX6-AS1) Biology medicine.disease_cause medicine.disease BMI1 Long non-coding RNA respiratory tract diseases non-small cell lung cancer (NSCLC) Oncology microRNA Cancer research medicine Original Article Radiology Nuclear Medicine and imaging Non small cell Carcinogenesis Lung cancer |
| Zdroj: | Translational Cancer Research |
| ISSN: | 2219-6803 2218-676X |
| Popis: | Background Non-small cell lung cancer (NSCLC) is a huge threat to sufferers’ life and overall health. Long non-coding RNA (lncRNA) distal-less homeobox 6 antisense RNA 1 (DLX6-AS1) has been revealed to function as a carcinogenesis factor in some cancers. This research aimed to scrutinize the role and mechanism underlying DLX6-AS1 in NSCLC tumorigenesis and progression. Methods The levels of DLX6-AS1, microRNA-16-5p (miR-16-5p), and BMI1 mRNA were estimated via reverse transcription-quantitative PCR (RT-qPCR) assay. The protein levels were disclosed by western blot assay. Cell proliferative potential was estimated by colony formation and Cell Counting Kit-8 (CCK-8) assays. Cell migration was estimated by Transwell and wound healing assay. A Transwell assay was executed to estimate cell invasion. The relationships of DLX6-AS1, miR-16-5p, and BMI1 were forecasted by bioinformatics analysis, and confirmed by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. A xenograft mice model was employed to to inspect the function of DLX6-AS1 knockdown on NSCLC tumorigenesis in vivo. Results DLX6-AS1 was overexpressed in NSCLC tissues and cells, and was inextricably linked with the poor prognosis of NSCLC patients. Depletion of DLX6-AS1 oppressed cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) but promoted apoptosis in NSCLC. MiR-16-5p is a target of DLX6-AS1 and directly targets BMI1. Moreover, the anti-tumor impacts of miR-16-5p were overturned by overexpression of DLX6-AS1 or BMI1 in NSCLC cells. Additionally, DLX6-AS1 silencing inhibited tumor growth of NSCLC in vivo. Conclusions In conclusion, lncRNA DLX6-AS1 downregulation suppressed the tumorigenesis and progression of NSCLC via miR-16-5p/BMI1 axis in vitro and in vivo, elucidating the vital roles and downstream targets of DLX6-AS1 in NSCLC. |
| Databáze: | OpenAIRE |
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