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Long non-coding RNA DDX11-AS1 promotes non-small cell lung cancer development via regulating PI3K/AKT signalling
Xuegang Feng1, Shengsheng Yang1, Shunkai Zhou1
1Department of Cardiothoracic Surgery, 900th Hospital of Joint Logistics Support Force of People's Liberation Army, Fuzhou, China.
Abstract:
Non-small cell lung cancer (NSCLC) has been considered to be the most common category of lung cancer, comprising approximately 80% of lung cancers. Long non-coding RNAs (lncRNAs) were diffusely documented to modulate carcinogenesis or progression of tumours. However, the role of DDX11-AS1 was still unclear in NSCLC. Bioinformatics analysis and experimental assays including hematoxylin and eosin (H&E) staining, RT-qPCR, colony formation, CCK-8, flow cytometry, western blot and xenograft assays were applied to investigate the biological role and molecular mechanism of DDX11-AS1 in NSCLC. The level of lncRNA DDX11-AS1 was up-regulated in NSCLC tumour tissues and cells. In function aspect, knockdown of DDX11-AS1 caused an apparent inhibitive effect on cell proliferation in vitro and in vivo. DDX11-AS1 inhibition promoted cell apoptosis in vitro. In mechanism, the protein level of phosphorylated AKT was reduced by DDX11-AS1 inhibition but increased by DDX11-AS1 overexpression. These results indicated that DDX11-AS1 exacerbated NSCLC progression via activating PI3K/AKT signalling pathway. All in all, DDX11-AS1 promotes NSCLC development via regulating PI3K/AKT signalling.
Insights
The long non-coding RNA DDX11-AS1 promotes non-small cell lung cancer (NSCLC) development. Inhibiting DDX11-AS1 suppresses NSCLC cell proliferation and enhances apoptosis by affecting the PI3K/AKT pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Non-small cell lung cancer (NSCLC) is the most common form of lung cancer.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer development.
- The specific role of DDX11-AS1 in NSCLC progression remained largely uncharacterized.
Purpose of the Study:
- To investigate the biological role of the lncRNA DDX11-AS1 in NSCLC.
- To elucidate the molecular mechanism underlying DDX11-AS1's function in NSCLC progression.
- To determine if DDX11-AS1 influences the PI3K/AKT signaling pathway.
Main Methods:
- Bioinformatics analysis and experimental assays including H&E staining, RT-qPCR, colony formation, CCK-8, flow cytometry, western blot, and xenograft assays.
- Assessing DDX11-AS1 expression levels in NSCLC tissues and cells.
- Evaluating the functional impact of DDX11-AS1 knockdown on NSCLC cell proliferation, apoptosis, and in vivo tumor growth.
- Investigating the effect of DDX11-AS1 on the PI3K/AKT signaling pathway.
Main Results:
- DDX11-AS1 expression was significantly upregulated in NSCLC tumor tissues and cells.
- Knockdown of DDX11-AS1 inhibited NSCLC cell proliferation both in vitro and in vivo.
- Inhibition of DDX11-AS1 promoted apoptosis in NSCLC cells.
- DDX11-AS1 regulates the phosphorylation of AKT, indicating activation of the PI3K/AKT signaling pathway.
Conclusions:
- DDX11-AS1 acts as an oncogenic lncRNA that promotes the progression of NSCLC.
- DDX11-AS1 exacerbates NSCLC development by activating the PI3K/AKT signaling pathway.
- Targeting DDX11-AS1 may represent a potential therapeutic strategy for NSCLC.
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