Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA093

Poster Communications

The Effect of Beta Adrenergic Agonist and Antagonists on Caspase 3, Caspase 8 and Caspase 9 Expression on K562 Chronic Myeloid Leukemia Cells.

B. AYDIN1, Z. Kanli1, Z. Gören2, H. Cabadak1

1. Biophysics, Marmara University School of Medicine, Istanbul, Istanbul, Turkey. 2. Pharmacology and Clinical Pharmacology, Marmara University School of Medicine, Istanbul, Turkey.

  • Caspase 3 ekspression in K562 cells

  • Caspase 8, 9 ekspression in K562 cells.

The β adrenergic receptors, a family of G-protein-coupled receptors that are activated by adrenergic catecholamines, can initiate a series of signaling cascades, thereby leading to multiple cell specific responses. Beta adrenergic receptor signaling had been demonstrated to promote breast cancer growth (1), recurrence and metastasis (2) and reduce apoptosis of cancer cells (3, 4). Some researchers demonstrated that β2 adrenergic receptor stimulation could significantly suppress the malignant transformation of cancers, cancer cell growth and proliferation by cutting of the Raf-1/Mek-1/Erk1/2 pathway (5). Chronic myeloid leukemia is a hematopoietic stem cell malignancy characterized by myeloid cell proliferation and loss of adhesive properties of the myeloid elements. K562 cell line was established by Lozzio et al., from a patient with chronic myeloid leukemia (CML) in terminal blast crisis (1975). Previously, we found that no difference of beta 1, beta 2 adrenergic receptor expression levels on human chronic myeloid leucemia K562 cells. In this study, we aimed to determine the expression levels of caspases 3, 8 and 9, which are effective on cell apoptosis pathway in the presence of isoprenaline and propranolol, in order to determine the role of β adrenoceptors in the apoptosis pathway of K562 cells. Methods K562 (ATCC No: CCL-243) chronic myeloid cells were harvested after 24 hours of treatment with agonist and / or antagonist. In these cell lysates caspase 3, 8, and 9 protein levels were determined by western immunoblotting. One-way ANNOVA and Bonfferoni post test statistical analyzes were used in the GraphPad Prism 5.0 program. Results Isoprenaline caused a decrease in caspase 3,8 and 9 expression compared to the control group. The propranolol has been shown to cause an increase in caspase 9 expression, leading to a decrease in caspase 3, 8 expression relative to control group. It would seem that propanolol triggers apoptosis through mitochondrial pathway in these cells as a result of the significant increase in caspase 9 expression due to propanolol. Key Words: G protein coupled receptors, cancer, isoprenaline, propranolol, protein expression

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