Resumen de Circ_0007385 promotes the proliferation and inhibits the apoptosis of non-small cell lung cancer cells via miR-337-3p-dependent regulation of LMO3

Mingchao Wei, Rongjiang Yin, Li Qu, Jian Tang

• Background. This study intended to analyze the expression characteristic, functions and underlying mechanism of circular RNA_0007385 (circ_0007385) in non-small cell lung cancer (NSCLC).

  Methods and Results. RNA and protein expression was examined by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot assay. Cell counting kit 8 (CCK8) assay, colony formation assay, 5- Ethynyl-2’-deoxyuridine (EdU) assay and flow cytometry were applied to analyze cell proliferation ability. Flow cytometry was also conducted to assess cell apoptosis. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the predicted target relationships. Xenograft tumor model was utilized to analyze the function of circ_0007385 in vivo, and immunohistochemistry (IHC) assay was used to analyze protein expression in xenograft tumor tissues. Circ_0007385 expression was notably enhanced in NSCLC tissues and cell lines.

  Circ_0007385 facilitated the proliferation but suppressed the apoptosis of NSCLC cells. Circ_0007385 acted as a sponge for microRNA-337-3p (miR-337-3p), and circ_0007385 overexpression-mediated effects were largely overturned by the overexpression of miR-337-3p in NSCLC cells. MiR-337-3p interacted with the 3’ untranslated region (3’UTR) of LIM-only protein 3 (LMO3). Circ_0007385 up-regulated LMO3 level by absorbing miR-337-3p in NSCLC cells. LMO3 overexpression largely reversed miR-337-3p overexpression-induced influences in NSCLC cells.

  Circ_0007385 knockdown significantly restrained the growth of xenograft tumors in vivo.

  Conclusion. Circ_0007385 promoted the proliferation ability and inhibited the apoptosis of NSCLC cells by binding to miR-337-3p to induce LMO3 expression.