LAUSR

Purpose LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and Methods Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.