Analysis of Thiosemi Carbazon Complexes Effects on UCA1 lncRNA andAKT Target, Gene Expression Alternations, Regulating PI3K / AKT SignalingPathway in Jurkat E6.1 Acute Lympholastic Leukemia Cell Line

Leukemia usually begins in the bone marrow and leads to the production ofa large number of abnormal white blood cells.The goal of this study was to investigate changes on UCA1lncRNA and AKT target, gene expression alternations, regulating PI3K / AKT signaling pathway in JurkatE6.1 Acute Lympholastic Leukemia cell line under treatment with thiosemicarbazone complexes (nickel).

First, thiosemicarbazones complex Ni and 6MP was provided in different concentrations(0.5,1,2,5 μM) and (1,5,10,25 μM) and the jurkat E.6.1 Cancer cells were treated with mentioneddoses at (24-48-72 hours) after cell passage. Next RNA extraction and cDNA synthesis were performedand the expression of UCA1 and AKT gene were appraised by Real Time PCR. Finally, the resultswere analyzed by Rest Software.

UCA1 showed a significant decrease during 24 hours of treatment with 6mp at concentrations(1,5,10 and 25 μM) (P<0.001). In nickel,a significant decrease at 72 hours was observed at concentrations(2 and 5 μM). In the AKT in treatment with 6mp at 24 hours At concentrations (5,10 and 25 μM)And all concentrations (1,5,10 and 25 μM) at 72 hours showed a significant decrease (P<0.001). In nickelat concentrations (0.5,1,2 and 5 μM) at 24 hours Decreased expression was observed, This decrease isnot statistically significant at a concentration of 0.5μM.at concentrations (2 and 5 μM) Significant reductionsat 48 and 72 hours were observed (P<0.001).

UCA1 and AKT expression changes after treatment with 6mp and nickel depend on drugtiming and concentration.UCA1 in 6MP treatment at 25μM and 24 hours,in treatment with nickel at5μM and 72 hours , AKT in 6mp treatment at 25μM and 72 hours , In treatment with nickel at 5μM and24hours,It had the highest effect on the cell due to gene expression.