Abstract
T cell acute lymphoblastic leukemia (T-ALL) is a high-risk malignancy. The effects of cancer growth-related Long Intergenic Non-Protein Coding RNA 665 (LINC00665) in T-ALL remained obscure, and therefore further exploration was conducted on that in this study. The expression of LINC00665 in acute myeloid leukemia (LAML) tissues and myeloid tissues was analyzed using Gene Expression Profiling Interactive Analysis (GEPIA) 2. The target microRNA (miR) of LINC00665 was predicted by LncBase Predicted v.2 and verified using dual-luciferase reporter assay. After LINC00665 and miR-101 in T-ALL cells were overexpressed or silenced, the viability, migration and invasion of cell were detected using cell counting kit-8 and Transwell assays. The expressions of LINC00665, miR-101, Cyclin D1, Matrix metalloproteinases (MMP)-2, MMP-9, phosphorylated (p)-phosphatidylinositol 3-kinase (PI3K), PI3K, p-Akt, Akt were detected by quantitative real-time Polymerase Chain Reaction (qRT-PCR) and western blot. High expression of LINC00665 was presented in LAML tissues, the peripheral blood samples from patients with T-ALL and T-ALL cells. Overexpression of LINC00665 promoted the viability, migration and invasion of T-ALL cells and downregulated miR-101 expression, whereas silencing of LINC00665 did oppositely. MiR-101 could competitively bind to LINC00665, and was low-expressed in T-ALL. MiR-101 mimic inhibited viability, migration and invasion of T-ALL cells, and reversed effects of overexpressed LINC00665, whilst miR-101 inhibitor reversed the effects of LINC00665 silencing. Besides, overexpressed LINC00665 upregulated the expressions of Cyclin D1 MMP-2, and MMP-9 and the ratios of p-PI3K/PI3K and p-Akt/Akt, which were reversed by miR-101 mimic. LINC00665 could enhance the viability, migration and invasion abilities of T-ALL cells by targeting miR-101 via activating PI3K/Akt pathway.
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