Abstract: Objective To investigate the role of Tal1 gene, which is aberrantly expressed in 40%-60% of patients with T
lymphocytic leukemia (T-ALL), in the proliferation of T-ALL cells. Methods We established stable Jurkat-siTal1 and Jurkat-T1
cell lines by trasnfecting T-ALL Jurkat cells with lentiviral vectors to knock-down or overexpress Tal1. Jurkat cells transfected
with negative control siRNAs for Tal1 knock-down (Jurkat-mock1) and over-expression(Jurkat-mock2) served as the control
cells. The proliferation of the cells lines was assessed using CCK-8 assay, and the cell cycle distribution was determined by
flow cytometry. The mRNA and protein expressions of cyclin-dependent kinase inhibitor 2 (CDKN2A) and cyclin-dependent
kinase inhibitor 1 (CDKN2B) were measured by real-time RT-PCR and Western blotting, respectively. Results Jurkat-T1 cells
showed more active proliferation in vitro than Jurkat-mock2 cells, while Jurkat-siTal1 cells showed slower growth than
Jurkat-mock1 cells. In Jurkat-T1 cells, G0/G1 phase cells were decreased and S phase cells increased compared with
Jurkat-mock2 cells, and Jurkat-siTal1 cells showed increased G0/G1 phase cells and decreased S phase cells compared with
Jurkat-mock1 cells. Real-time RT-PCR and Western blotting showed that Tal1 inhibited the cellular expression of CDKN2A and
CDKN2B at both mRNA and protein levels. Conclusion Tal1 promotes the growth and the transition from G0/G1 phase to S
phase in T-ALL cells Jurkat by inhibiting the expressions of G0/G1 and S phase negative regulatory proteins CDKN2A and
CDKN2B.