ArticleTranslational cancer research2021
Long non-coding RNA DLX6-AS1 knockdown suppresses the tumorigenesis and progression of non-small cell lung cancer through microRNA-16-5p/BMI1 axis.
Article in Translational cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification of Genomic Instability-Associated LncRNAs as Potential Therapeutic Targets in Lung Adenocarcinoma.Cancers · 2025Article
- The lncRNA DLX6-AS1/miR-16-5p axis regulates autophagy and apoptosis in non-small cell lung cancer: A Boolean model of cell death.Non-coding RNA research · 2023Article
- Hsa_circ_0102899 promotes epithelial-mesenchymal transition in non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Various LncRNA Mechanisms in Gene Regulation Involving miRNAs or RNA-Binding Proteins in Non-Small-Cell Lung Cancer: Main Signaling Pathways and Networks.International journal of molecular sciences · 2023Review
- METTL3-induced DLGAP1-AS2 promotes non-small cell lung cancer tumorigenesis through mCell cycle (Georgetown, Tex.) · 2022Article
- Strategies of LncRNA DLX6-AS1 on Study and Therapeutics.Frontiers in genetics · 2022Review
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-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.
methodsThe 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
resultsDLX6-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
conclusionsIn conclusion, lncRNA DLX6-AS1 downregulation suppressed the tumorigenesis and progression of NSCLC via miR-16-5p/BMI1 axis
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