Long non-coding RNA LINC00339 facilitates the tumorigenesis of non-small cell lung cancer by sponging miR-145 through targeting FOXM1

[Display omitted] •LINC00339 was significantly up-regulated in NSCLC tissue and cells, which indicated the poor prognosis of NSCLC patients.•LINC00339 silencing inhibited the proliferation and invasion, accelerated the apoptosis, and suppressed the tumor growth of NSCLC cells.•Luciferase assay and R...

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Veröffentlicht in:Biomedicine & pharmacotherapy 2018-09, Vol.105, p.707-713
Hauptverfasser: Yuan, Yuan, Haiying, Gao, Zhuo, Li, Ying, Lu, Xin, He
Format: Artikel
Sprache:eng
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Zusammenfassung:[Display omitted] •LINC00339 was significantly up-regulated in NSCLC tissue and cells, which indicated the poor prognosis of NSCLC patients.•LINC00339 silencing inhibited the proliferation and invasion, accelerated the apoptosis, and suppressed the tumor growth of NSCLC cells.•Luciferase assay and RIP confirmed that LINC00339 promoted the NSCLC progression via FOXM1-miR-145. Non-small cell lung cancer (NSCLC) is one of leading causes of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) has been identified to modulate the tumorigenesis of NSCLC. However, the precise molecular mechanism of lncRNAs in the course is still unclear. Results showed that LINC00339 was significantly up-regulated in NSCLC tissue and cells, which indicated the poor prognosis of NSCLC patients. Loss-of-function experiments showed that LINC00339 silencing inhibited the proliferation and invasion, accelerated the apoptosis, and suppressed the tumor growth of NSCLC cells in vitro and in vivo. Luciferase reporter assay and RNA immunoprecipitation (RIP) revealed that LINC00339 promoted the NSCLC progression via FOXM1 via targeting miR-145. In conclusion, our results identify the important role of the LINC00339/miR-145/FOXM1 axis in the NSCLC tumorigenesis, providing neoteric mechanism for the NSCLC tumorigenesis.
ISSN:0753-3322
1950-6007
DOI:10.1016/j.biopha.2018.06.022