LncRNA FOXP4-AS promotes the progression of non-small cell lung cancer by regulating the miR-3184-5p/EIF5A axis.
Dingbiao LiZhenhua LiWang YanFeiYing WangJianlin ShiChang LiuLaihao QuShoujun DengDalin XiongPublished in: Journal of tissue engineering and regenerative medicine (2022)
Long non coding RNA FOXP4-AS1 exerted crucial functions in various human cancers, while its role in non-small cell lung cancer (NSCLC) remains unclear. A total of 30 pairs of NSCLC tissues and matched adjacent normal tissues were used to evaluate the expression of FOXP4-AS1 and miR-3184-5p. Cell proliferation was assessed by CCK-8 assay and colony formation assay. Cell apoptosis was measured by flow cytometry. Bioinformatic analysis and luciferase reporter assay were performed to determine the regulatory relationship among FOXP4-AS1, miR-3184-5p and EIF5A. The xenograft tumor model was constructed to confirm the function of FOXP4-AS1 in NSCLC progression. The results showed that FOXP4-AS1 was upregulated and miR-3184-5p was downregulated in NSCLC tissues and cell lines. Downregulation of FOXP4-AS1 significantly reduced cell proliferation and induced apoptosis of NSCLC cells in vitro. FOXP4-AS1 could regulated the expression of EIF5A by binding to miR-3184-5p. Rescue experiments showed that downregulation of miR-3184-5p or overexpression of EIF5A obviously attenuated the inhibitory effects of si-FOXP4-AS1 on cell proliferation, as well as the stimulating effects on cell apoptosis. Moreover, knockdown of FOXP4-AS1 could efficiently inhibited tumor development of NSCLC in vivo. Downregulation of FOXP4-AS1 attenuated the progression of NSCLC by regulating miR-3184-5p and EIF5A.
Keyphrases
- regulatory t cells
- cell proliferation
- small cell lung cancer
- induced apoptosis
- long non coding rna
- poor prognosis
- advanced non small cell lung cancer
- dendritic cells
- signaling pathway
- gene expression
- cell cycle
- high throughput
- endoplasmic reticulum stress
- oxidative stress
- brain metastases
- endothelial cells
- pi k akt
- transcription factor
- wastewater treatment
- cell cycle arrest
- binding protein
- young adults