https://www.selleckchem.com/products/acetohydroxamic-acid.html Based on the loss-of-function experiments, silencing expression significantly inhibited malignancy progression. In terms of the mechanism, acted on the ( ) by direct binding, which promoted BC cell growth. Furthermore, in the promoters of , the trimethylation of could be regulated by as the mediator. Relying on the / / pathway, the lncRNA was significantly associated with BC development and could, therefore, be a potential therapeutic target to block BC growth. Relying on the LL22NC03-N64E9.1/EZH2/KLF2 pathway, the lncRNA LL22NC03-N64E9.1 was significantly associated with BC development and could, therefore, be a potential therapeutic target to block BC growth. Non-small cell lung cancer (NSCLC) is a common malignant tumor in humans. Long non-coding RNA (lncRNA) involved in cancer progression has been reported frequently. The objective of this study was to investigate the role of lncRNA metastasis-associatedlung adenocarcinoma transcript 1 (MALAT1) and explore a novel mechanism in NSCLC development. The expression of MALAT1, copper metabolism MURR1 domain-containing 8 ( ) and microRNA-613 (miR-613) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of COMMD8, Cyclin D1, Ki67, B cell lymphoma/leukemia-2 (Bcl-2), Bcl-2 associated X protein (Bax), lactate dehydrogenase A (LDHA), CD63 and CD81 were determined by Western blot. Cell proliferation, the number of colonies and cell apoptosis were assessed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation and flow cytometry assays, respectively. Glycolysis was distinguished based on glucose consumption, lactate production and LDHA acproach for NSCLC treatment. MALAT1 promoted malignant activities of NSCLC cells through targeting miR-613/COMMD8 axis, and exosome-mediated transfer of NSCLC might be a novel approach for NSCLC treatment. is one of the genes identified as a prolife