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Updated: Oct 4, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Long non-coding RNA DLX6-AS1 knockdown suppresses the tumorigenesis and progression of non-small cell lung cancer
Chengde Wu1, Wei Lin1, Fangyong Fu1
1Department of Thoracic Surgery, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou People's Hospital, Haidian Island, Haikou, China.
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.
Insights
Downregulating long non-coding RNA DLX6-AS1 inhibits non-small cell lung cancer (NSCLC) progression by targeting the microRNA-16-5p/BMI1 pathway. This finding offers a potential therapeutic strategy for NSCLC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) poses a significant health burden.
- Long non-coding RNA (lncRNA) DLX6-AS1 is implicated in various cancers.
- The specific role of DLX6-AS1 in NSCLC tumorigenesis requires elucidation.
Purpose of the Study:
- To investigate the role and underlying mechanism of DLX6-AS1 in NSCLC.
- To determine the relationship between DLX6-AS1, microRNA-16-5p (miR-16-5p), and BMI1 in NSCLC.
Main Methods:
- Quantitative PCR (qPCR) and Western blot for molecular level analysis.
- Cell proliferation, migration, invasion, and apoptosis assays for functional characterization.
- Bioinformatics, luciferase reporter, and RNA immunoprecipitation (RIP) assays to confirm molecular interactions.
- In vivo xenograft mouse model to assess DLX6-AS1's effect on tumor growth.
Main Results:
- DLX6-AS1 was upregulated in NSCLC tissues and correlated with poor prognosis.
- DLX6-AS1 depletion suppressed NSCLC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while promoting apoptosis.
- DLX6-AS1 acts as a sponge for miR-16-5p, which directly targets BMI1.
- DLX6-AS1 silencing inhibited tumor growth in vivo.
Conclusions:
- lncRNA DLX6-AS1 downregulation suppresses NSCLC tumorigenesis and progression.
- The miR-16-5p/BMI1 axis is a key downstream pathway regulated by DLX6-AS1 in NSCLC.
- DLX6-AS1 is a potential therapeutic target for NSCLC.
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