Long non‑coding RNA linc00239 promotes malignant behaviors and chemoresistance against doxorubicin partially via activation of the PI3K/Akt/mTOR pathway in acute myeloid leukaemia cells

Abstract

Long non-coding RNAs (lncRNAs) are known to be involved in the processes of tumourigenesis and malignant behaviours in many types of cancer, including acute myeloid leukaemia (AML). Accumulating evidence has revealed that novel lncRNAs exerted critical roles in these processes. In the present study, we investigated the effects of lncRNA linc00239 (NR_026774.1), which is 662 nucleotides (nt) in length and was found to be upregulated in AML patients, on malignant behaviours and chemosensitivity in AML cells, including KG-1 and HL-60. linc00239 expression was detected in KG-1 and HL-60 cells by quantitative PCR and northern blotting, and it was found that linc00239 is detectable by both of these assays. After knockdown or overexpression of linc00239 in AML cells, the results revealed that the presence of linc00239 promoted proliferation, colony formation and migration ability. Furthermore, the presence of linc00239 increased chemoresistance to doxorubicin in AML cells partially by preventing doxorubicin-induced apoptotic cell death. It was also determined that the presence of linc00239 was related to activation of the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. Inhibition of PI3K/Akt/mTOR using 1 µM NVP-BEZ235 (BEZ) abolished the inhibitory effect of linc00239 on chemosensitivity and the preventative effect on doxorubicin-induced cell death. Collectively, our data revealed that linc00239 is a novel tumour promoter in AML cells and indicated that it is a potential therapeutic target.