Abstract.It has previously been demonstrated that the long non-coding RNA (lncRNA) nuclear enriched abundant transcript (NEAT)-1 is increased in multiple cancers and may be associated with cancer development. However, the function and mechanism of NEAT1 in non-small cell lung cancer (NSCLC) has not yet been fully elucidated. In the present study, the expression of NEAT1 in NSCLC was detected using quantitative polymerase chain reaction and association with survival was estimated. The effect of NEAT1 on proliferation was detected by growth curve and cell cycle analysis. Bioinformatics analysis was used to identify miRNAs that interact with NEAT1. Following this, a series of molecular biological techniques were used to verify the mechanism of NEAT1. The results indicated that NEAT1 was highly expressed in NSCLC, and high NEAT1 expression was associated with a shorter overall survival. NEAT1 promoted NSCLC cell growth and affected the cell cycle process in vitro. Furthermore, NEAT1 was observed to bind hsa-miR-377-3p, functioning as a competing endogenous RNA, which resulted in de-repression of its target gene E2F transcription factor 3 (E2F3). E2F3, as an oncogene, may promote NSCLC progression. These results suggested that NEAT1 may promote the development of NSCLC through the miR-377-3p-E2F3 pathway.

Oligo(ethylene glycol)-linked light fluorous tags have been found to be optimal for conjugating to glycans for both high-yield enzymatic glycosylation reactions using one-pot multienzyme (OPME) systems and quick product purification using fluorous solid-phase extraction (FSPE) cartridges. The combination of OPME glycosylation systems and the FSPE cartridge purification scheme provides a highly effective strategy for facile synthesis and purification of glycans.

Xeroderma pigmentosum, complementation group C (XPC) is an accessory recognition gene involved in the nucleotide excision repair (NER) pathway, which is activated during the initial DNA damage recognition stage. It participates in the regulation of DNA damage-induced proliferation and apoptosis. Emerging evidence demonstrates that upregulation of XPC increases the resistance of several tumor cell types to cytotoxic drugs. In addition, it can predict poor patient outcome for non-small cell lung cancer (NSCLC). However, the mechanisms linking upregulation of XPC and drug resistance in lung cancer are still unclear. In the present study, we aimed to confirm whether XPC was involved in the reversal of the cisplatin (DDP) resistance in drug-resistant A549/DDP lung adenocarcinoma cells. RT-PCR and western blot assays were used to examine XPC mRNA and protein expression levels. Cell viability was assessed by CCK-8 assay. The knockdown of XPC was achieved in A549/DDP cells using si-RNA, whereas cell proliferation and apoptosis were assessed by wound healing assay and flow cytometric analysis, respectively. The median inhibitory concentration (IC 50 ) value of DDP was assessed by CCK-8 assay. Western blot assays were conducted for the examination of caspase-9/3, Bax and Bcl-2 protein levels, whereas the activation of the PI3K/Akt/mTOR signaling pathway was investigated in XPC-knockdown cells. High expression of XPC was noted in A549/DDP cells compared with that in A549 cells, which was associated with DDP resistance. XPC silencing significantly inhibited A549/DDP cell proliferation and increased the induction of apoptosis. In addition, XPC knockdown decreased the expression levels of the Akt/mTOR signaling proteins and the expression of their downstream mediator. The data of the present study revealed that XPC inhibition rescued DDP resistance in lung adenocarcinoma cells, which was dependent on the Akt/mTOR signaling pathway. Collectively, XPC may be considered a new strategy for curing DDP-resistant lung cancer and may improve the efficacy of conventional chemotherapy.

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