title: Overexpression of Aiolos in Nalm-6 acute lymphoblastic leukaemia cells reduces apoptosis by suppressing phosphatase and tensin homologue deleted on chromosome 10 and activating the phosphatidylinositol-3-kinase/Akt signalling pathway.
abstract: The aim of the present study was to elucidate the molecular mechanism of Aiolos in the regulation of B‑cell leukaemia. A lentiviral system was used for overexpression of the Aiolos gene in Nalm‑6 cells to determine the effects of Aiolos on proliferation, apoptosis and the cell cycle. The expression and activation of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and Akt were also investigated. Upregulation of Aiolos inhibited cell growth and arrested an increased number of Nalm‑6 cells at the G0/G1 phase. The apoptotic cell quantities were also significantly lower in the Aiolos‑transfected Nalm‑6 cells. In addition, Aiolos overexpression downregulated PTEN, but increased the expression and phosphorylation of Akt in the Nalm‑6 cells. The Akt inhibitor, Akti‑1/2, reduced the percentage of viable Aiolos‑overexpressed Nalm‑6 cells, however, it had no effect on cell cycle arrest or proliferation. Aiolos upregulation in the Nalm‑6 cells inhibited cell proliferation, suppressed apoptosis and arrested the cell cycle at the G0/G1 phase. Aiolos improved the survival of Nalm‑6 cells via PTEN‑ and Akt‑dependent processes.
authors.affiliation: Department of Hematology, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Ran
authors.initials: R
authors.lastname: Wang
authors.affiliation: Cryomedicine Laboratory, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Gang
authors.initials: G
authors.lastname: Guo
authors.affiliation: Department of Hematology, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Hao
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Hematology, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Xiangxin
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Hematology, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yu
authors.affiliation: Cryomedicine Laboratory, Qilu Hospital, Shandong University, Ji'nan, Shandong 250012, P.R. China.
authors.forename: Dong
authors.initials: D
authors.lastname: Li
mesh_terms: D017209:Apoptosis / Q000235:genetics*; D059447:Cell Cycle Checkpoints / Q000235:genetics; D045744:Cell Line, Tumor; D002879:Chromosomes, Human, Pair 10; D017353:Gene Deletion; D015870:Gene Expression; D015973:Gene Expression Regulation, Leukemic; D006801:Humans; D051740:Ikaros Transcription Factor / Q000235:genetics*; D008840:Microfilament Proteins / Q000235:genetics*; D051059:PTEN Phosphohydrolase / Q000235:genetics / Q000378:metabolism; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D054198:Precursor Cell Lymphoblastic Leukemia-Lymphoma / Q000235:genetics* / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism; D015398:Signal Transduction; D000070876:Tensins; D014162:Transfection
chemical_list: C106285:IKZF3 protein, human; D008840:Microfilament Proteins; D047428:Protein Kinase Inhibitors; D000070876:Tensins; D051740:Ikaros Transcription Factor; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt; D051059:PTEN Phosphohydrolase