Erratum: Tg737 inhibition results in malignant transformation in fetal liver stem/progenitor cells by promoting cell-cycle progression and differentiation arrest

2011 ◽  
Vol 51 (10) ◽  
pp. 843-843
Author(s):  
Nan You ◽  
Weihui Liu ◽  
Xiao Zhong ◽  
Ru Ji ◽  
Ming Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Malignant Transformation ◽  
Cell Cycle Progression ◽  
Fetal Liver ◽  
Cycle Progression

scholarly journals Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells

Leukemia ◽  
2012 ◽  
Vol 27 (5) ◽  
pp. 1127-1138 ◽  
Author(s):  
O S Kustikova ◽  
A Schwarzer ◽  
M Stahlhut ◽  
M H Brugman ◽  
T Neumann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Cycle Progression

Cell cycle progression is required for nuclear migration of neural progenitor cells

2006 ◽  
Vol 1088 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Masaki Ueno ◽  
Kei-ichi Katayama ◽  
Hirofumi Yamauchi ◽  
Hiroyuki Nakayama ◽  
Kunio Doi
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Neural Progenitor Cells ◽  
Nuclear Migration ◽  
Neural Progenitor ◽  
Cycle Progression

scholarly journals Nucleophosmin Regulates Cell Cycle Progression and Stress Response in Hematopoietic Stem/Progenitor Cells

2006 ◽  
Vol 281 (24) ◽  
pp. 16536-16545 ◽  
Author(s):  
June Li ◽  
Daniel P. Sejas ◽  
Reena Rani ◽  
Tara Koretsky ◽  
Grover C. Bagby ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stress Response ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Hematopoietic Stem

Nucleophosmin Regulates Differentiation, Cell Cycle Progression, and Stress Response in Hematopoietic Progenitor Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 312-312
Author(s):  
June Li ◽  
Daniel P. Sejas ◽  
Qishen Pang
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Stress Response ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Proliferative Potential ◽  
Hematopoietic Progenitors ◽  
Cycle Progression ◽  
Hematopoietic Stem ◽  
Empty Vector

Abstract Nucleophosmin (NPM) is a multifunctional protein frequently overexpressed in actively proliferating cells including tumor and hematopoietic stem cells. Strong evidence indicates that NPM is involved in hematopoiesis and leukemic development. Here we report that NPM enhances the proliferative potential of hematopoietic stem/progenitor cells and increases cell survival upon stress challenge. Specifically, lin-Sca1+c-kit+ bone marrow cells transduced with retroviral vector expressing NPM exhibited higher proliferative rates in both short-term liquid culture and clonogenic progenitor cell assays, compared to the cells transduced with empty vector. Interestingly, NPM overexpression appears to inhibit differentiation of myeloid progenitors. Hematopoietic stem/progenitor cells infected with the NPM retrovirus expressed significantly lower levels of mature cell markers Gr-1 and Mac-1 compared to empty vector transduced cells, and majority of the NPM-overexpressing cells remained Sca1+C-Kit+ during the 5-day culture. Bone marrow transplantation experiments demonstrated that NPM overexpression increases long-term multi-lineage repopulating capacity of hematopoietic progenitors. We have not observed any evidence of proliferative disorders or leukemia in recipients transplanted with NPM-expressing progenitors thus far (4 months posttransplantation). Through cell-cycle profile analysis and single-cell division experiments, we showed that NPM overexpression induces rapid entry of hematopoietic progenitors into the cell cycle, probably via promoting G0/G1 to S transition. Furthermore, immunocytochemical and Western-blot analyses demonstrated that NPM-transduced cells expressed higher level of cyclin A compared to vector-transduced cells. Finally, overexpression of NPM significantly increased the survival of hematopoietic progenitors exposed to mitomycin C or hydrogen peroxide, suggesting that NPM can protect cells from DNA damage and oxidative stress. Together, these results indicate that NPM plays an important role in hematopoiesis via mechanisms involving modulation of progenitor differentiation, cell cycle progression, and stress response.

Induction of CABLES1 by the TKI Inhibits the Cell Cycle Progression and Induces Apoptosis In CML Cell.

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 1199-1199
Author(s):  
Tomonari Takemura ◽  
Satoki Nakamura ◽  
Yasuyuki Nagata ◽  
Daisuke Yokota ◽  
Isao Hirano ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Progenitor Cells ◽  
Cell Lines ◽  
Cell Cycle Progression ◽  
Kinase Inhibitors ◽  
Cycle Progression ◽  
Abl Kinase ◽  
Abl Kinase Inhibitors

Abstract Abstract 1199 [Background and Aims] CABLES1 (cyclin-dependent kinase (CDK)-5 and ABL enzyme 1) is a regulator of cell proliferation, apoptosis, and cell cycle, and it has been reported to be lost in a variety cancers. It has been also reported that knockout of the Cable1 gene has minimal to no effect on hematopoietic stem cells. However, we found that the expression of Cables1 gene and CABLES1 protein was suppressed in CML cells, and its function is little known in CML. In this study, we have investigated the function of CABLES1 in CML cell proliferation. [Methods] The cells used in this study were human CML cell lines, K562, Meg01 and SHG3 cells. Primary CML cells (ALDHhi cells) were obtained from the bone marrow of CML (CP) patients (n=12). Human normal ALDHhi cells were isolated from bone marrow of healthy volunteers after obtaining informed consents. For analysis of Cables1 mRNA expression, quantitative RT-PCR was performed in all cell lines treated with Abl kinase inhibitors (STI571, AMN107, and BMS354825). For cell survival analysis and the levels of p53 and some CDKIs in CML cells, MTT assays, western blot and cell cycle analysis were performed in all cell lines transfected with Cables1 shRNA or cDNA. For colony analysis, the colonies of CFU-GEMM, CFU-GM, and BFU-E were counted in CML stem/progenitor cells transfected with Cables1 cDNA or shiRNA, or treated with Abl kinase inhibitors. [Results] In CML cell lines, the expressions of Cables1 mRNA and CABLES1 protein were significantly increased by treatment with Abl kinase inhibitors or transfection with Bcr-Abl shRNA. In CML cells transfected with the Cables1 cDNA, it is shown that CML cell proliferation was inhibited, and the phosphorylation levels of p53, and the expression of BAX and p21 protein were markedly increased compared to the untransfected cells. In addition, the overexpression of CABLES1 induced G1 cell cycle arrest and reduced the DiOC6 fluorescence, indicating breakdown of the mitochondrial membrane potential in CML cells. On the other hand, the changes of p73 and p27 protein expression were not detected. Moreover, in CML cells transfected with Cables1 shRNA, the inhibition of CML cell proliferation by the Abl kinase inhibitors were weakened. In CML stem/progenitor cells (ALDHhi cells) obtained from patients with CML, the expression of Cables1 mRNA was suppressed, and the transfection with Bcr-Abl shRNA or treatment with Abl kinase inhibitors increased the expression of Cables1 mRNA and CABLES1 protein, and decreased the counts of CFU-GEMM, CFU-GM and BFU-E. [Conclusion] Our results demonstrated that the Bcr-Abl suppressed the expression of CABLES1, and the depletion of CABLES1 promotes cell cycle progression and p53-dependent apoptosis. Moreover, the induction of CABLES1 expression has the potentiality to eradicate CML stem/progenitor cells. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Malnutrition suppresses cell cycle progression of hematopoietic progenitor cells in mice via cyclin D1 down-regulation

Nutrition ◽  
2014 ◽  
Vol 30 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Karina Nakajima ◽  
Amanda R. Crisma ◽  
Graziela B. Silva ◽  
Marcelo M. Rogero ◽  
Ricardo A. Fock ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Down Regulation ◽  
Cycle Progression

scholarly journals Sex Differences of Human Cardiac Progenitor Cells in the Biological Response to TNF-α Treatment

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Elisabetta Straface ◽  
Lucrezia Gambardella ◽  
Francesca Pagano ◽  
Francesco Angelini ◽  
Barbara Ascione ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Intracellular Signaling ◽  
Cell Cycle Progression ◽  
Present Report ◽  
Cardiac Progenitor Cells ◽  
Regenerative Therapy ◽  
Migration Ability ◽  
Differentiation Potential ◽  
Cycle Progression

Adult cardiac progenitor cells (CPCs), isolated as cardiosphere-derived cells (CDCs), represent promising candidates for cardiac regenerative therapy. CDCs can be expanded in vitro manyfolds without losing their differentiation potential, reaching numbers that are appropriate for clinical applications. Since mechanisms of successful CDC survival and engraftment in the damaged myocardium are still critical and unresolved issues, we aimed at deciphering possible key factors capable of bolstering CDC function. In particular, the response and the phenotype of CDCs exposed to low concentrations of the multifunctional cytokine tumor necrosis factor α (TNF-α), known to be capable of activating cell survival pathways, have been investigated. Furthermore, differential biological responses of CDCs from male and female donors, in terms of cell cycle progression and cell spreading, have also been assessed. The results obtained indicate that (i) the intracellular signaling activated in our experimental conditions is most likely due to the prosurvival and proliferative signaling of TNF-α receptor 2 and that (ii) cells from female patients appear more responsive to TNF-α treatment in terms of cell cycle progression and migration ability. In conclusion, the present report highlights the hypothesis that TNF-stimulated CDCs isolated from females may represent a promising candidate for cardiac regenerative therapy applications.

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