Growth Of Human Myeloid Leukemia Cells Research Articles

Inhibitory Effect of Cell Phones Against Human Breast Cancer and Myeloid Leukemia Cells Proliferation in Culture Media

Objective: There is current news that emerges regarding the relationship between the magnetic effects of cell phones and some types of cancer. In spite of the studies carried out, the level of evidence of this news is low, and also the relationship between the magnetic effects of cell phones and other types of cancer is not certain except for brain cancer. In this study, it is aimed at examining the effects of magnetic field of cell phones on the samples of breast cancer human myeloid leukemia cell growth. 
 Methods: In the study, breast cancer MCF-7 and leukemia K562 cell lines were used as the source of cancer cell. During the six-day cell culture, cancer cells were subjected to the effects of cell phone by using a telephone call program (Automated outbound call software). The system made 6 calls for 1 minute for each call once in 144 minutes from fixed line. The number of cultured cells and proliferation capacities of the two types of tumor cells in the control and experimental groups were assessed. 
 Results: The number of cancer cells, which were subjected to the effects of cell phone as a result of the culture of tumor cells, was found lower when compared with control group (7500000 ± 100000 vs 6625000 ± 225000 for MCF-7; 15412500 ± 112500 vs 13700000 ± 250000 for K562; P < 0.05 for both). In MTT test, it was found out that two types of cell proliferation was inclined to slow down with the effect of cell phone. 
 Conclusion: The results can be translated that cell phone may inhibit neoplastic transformation, and this observation may promote to initiate a new clinical studies both for healthy people and for patients with cancer.

Olfactomedin 4 is a novel target gene of retinoic acids and 5-aza-2′-deoxycytidine involved in human myeloid leukemia cell growth, differentiation, and apoptosis

AbstractClinical application of retinoic acids (RAs) and demethylation agents has proven to be effective in treating certain myeloid leukemia patients. However, the target genes that mediate these antileukemia activities are still poorly understood. In this study, we identified olfactomedin 4 (OLFM4), a myeloid-lineage–specific gene from the olfactomedin family, as a novel target gene for RAs and the demethylation agent, 5-aza-2′-deoxycytidine. We demonstrated that the retinoic acid receptor alpha/retinoic X receptor alpha heterodimer binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-retinoic acid (ATRA)–induced transactivation of the OLFM4 gene. OLFM4 overexpression in HL-60 cells led to growth inhibition, differentiation, and apoptosis, and potentiated ATRA induction of these effects. Conversely, down-regulation of endogenous OLFM4 in acute myeloid leukemia-193 cells compromised ATRA-induced growth inhibition, differentiation, and apoptosis. Overexpression of OLFM4 in HL-60 cells inhibited constitutive and ATRA-induced phosphorylation of the eukaryote initiation factor 4E-binding protein 1 (4E-BP1), whereas down-regulation of OLFM4 protein in acute myeloid leukemia-193 cells increased 4E-BP1 phosphorylation, suggesting that OLFM4 is a potent upstream inhibitor of 4E-BP1 phosphorylation/deactivation. Thus, our study demonstrates that OLFM4 plays an important role in myeloid leukemia cellular functions and induction of OLFM4-mediated effects may contribute to the therapeutic value of ATRA.

Growth-inhibitory effects of transforming growth factor- β1 on myeloid leukemia cell lines

Transforming growth factor- β1 is a pleiotropic cytokine involved in a variety of biological processes in both transformed and normal cells, including regulation of cellular proliferation and differentiation; its predominant action on hematopoietic cells is to inhibit cell growth. We used growth factor-dependent cell lines to assess TGF- β1 effects on human myeloid leukemia cell growth. While four lines were completely or predominantly resistant, TGF- β1 inhibited effectively, albeit to various extents, the growth of 12 other cell lines. This effect was dose dependent and specific, because a neutralizing anti-TGF- β1 antibody prevented TGF- β1-induced growth suppression. In the present system, basic fibroblast growth factor, known as an antagonist of TGF- β1 counteracting its inhibitory effects, did not abrogate the suppressive effects of TGF- β1. Other growth-stimulatory cytokines negated the TGF- β1-induced inhibition in several cell lines, again to various extents. When proliferation was enhanced by growth-promoting cytokines (e.g. granulocyte-macrophage colony-stimulating factor, GM-CSF, stem cell factor, SCF, or PIXY-321), some previously TGF- β1-sensitive cell lines acquired cellular resistance toward TGF- β1-mediated growth suppression, whereas four other cell lines remained susceptible to TGF- β1 growth inhibition despite possible counteraction by other cytokines. Thus, three growth response patterns to TGF- β1 were seen: (1) constitutive resistance; (2) factor-dependent relative resistance; and (3) sensitivity to growth inhibition indifferent to counteracting cytokines. In the latter case, TGF- β1 did not downregulate expression of one specific growth factor receptor. These studies indicate that human myeloid leukemia cells, represented here by leukemia cell lines as model systems, exhibit heterogeneous growth responses to TGF- β1; its inhibitory effects can be modulated or completely alleviated by positive antagonistic cytokines. The availability of TGF- β1-susceptible and -refractory cell lines allows for detailed investigations on the mechanisms of these regulatory pathways, the nature of TGF- β1-resistance, and the possible contribution of acquired TGF- β1-resistance to disease progression.