title: [Tal1 promotes proliferation of acute lymphoblastic leukemia Jurkat cells in vitro].
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Center for Clinical Molecular Medicine, Children's Hospital of Chongqing Medical University/Ministry of Education Key Laboratory of Child Development and Disorders/Key Laboratory of Pediatrics in Chongqing/Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Chongqing 400014, China.E-mail: 641807153@qq.com.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
authors.forename: Yi
authors.initials: Y
authors.lastname: Shu
authors.forename: Juntao
authors.initials: J
authors.lastname: Yuan
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Lin
authors.initials: L
authors.lastname: Zou
mesh_terms: D017209:Apoptosis; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism*; D002453:Cell Cycle; D049109:Cell Proliferation; D050762:Cyclin-Dependent Kinase Inhibitor p15 / Q000378:metabolism; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D006801:Humans; D019169:Jurkat Cells; D016086:Lentivirus; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000378:metabolism* / Q000473:pathology; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D034741:RNA, Small Interfering; D000073942:T-Cell Acute Lymphocytic Leukemia Protein 1
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D050762:Cyclin-Dependent Kinase Inhibitor p15; D019941:Cyclin-Dependent Kinase Inhibitor p16; D011518:Proto-Oncogene Proteins; D034741:RNA, Small Interfering; D000073942:T-Cell Acute Lymphocytic Leukemia Protein 1; C493966:CDKN2B protein, human; C067143:TAL1 protein, human