Long non-coding RNA FLVCR1-AS1 contributes to the proliferation and invasion of lung cancer by sponging miR-573 to upregulate the expression of E2F transcription factor 3.

Lung cancer is one of the most common causes of cancer-related death all over the world. In recent years, long non-coding RNAs (lncRNAs) have been reported to play critical roles in the development and progression of human malignancies. In the present study, we aimed to study the role and mechanism of FLVCR1-AS1 in human non-small cell lung cancer (NSCLC). Results revealed that FLVCR1-AS1 was markedly upregulated in NSCLC tissues and cell lines. Knockdown of FLVCR1-AS1 significantly inhibited the proliferation, migration, invasion and promoted apoptosis of NSCLC cells, and suppressed tumor growth of NSCLC in vivo. Moreover, we explored regulatory mechanism, and found that FLVCR1-AS1 functioned as a competing endogenous RNA (ceRNA) by directly binding to miRNA-573, and E2F transcription factor 3 (E2F3) was identified as a down-stream target of miR-573. FLVCR1-AS1 positively regulated E2F3 expression through inhibiting miR-573 in NSCLC cells. Our findings suggested that FLVCR1-AS1/miR-573/E2F3 axis was an important signaling pathway in mediating tumorigenesis and progression of NSCLC, and further indicated that FLVCR1-AS1 could be a novel diagnostic biomarker and therapeutic target for NSCLC.

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