https://www.selleckchem.com/pr....oducts/20-hydroxyecd
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
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