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Prognostic role of sensitive-to-apoptosis gene expression in rectal cancer
(BAISHIDENG PUBL GRP CO LTD, 2011-01-01) Ozden, Sevgi A.; Ozyurt, Hazan; Ozgen, Zerrin; Kilinc, Olca; Oncel, Mustafa; Gul, Aylin E.; Karadayi, Nimet; Serakinci, Nedime; Kan, Beki; Orun, Oya
AIM: To investigate the association between prognosis of rectal cancer treated with chemoradiotherapy (CRT) and expression of sensitive-to-apoptosis (SAG), B-cell lymphoma-extra large (Bcl-XL) and Bcl-2 homologous antagonist/killer (Bak). METHODS: Real-time quantitative polymerase chain reaction was used to determine the expression of proteins of interest, namely SAG, Bcl-XL, Bak and beta-actin, in rectal carcinoma patients who had a follow-up period of 3 years after CRT. Biopsy specimens were excised from the rectal tumor preceding CRT. RESULTS: SAG, Bcl-XL and Bak proteins showed significant correlations with each other. In multivariate analysis, patients with high vs low SAG expression showed a statistically significant difference in 2-year survival rates: 56\% vs 73\%, respectively (P = 0.056). On the other hand, there were no significant correlations between the expression levels of all three genes and metastatic rates or tumor responses to CRT. Mean overall survival in the patients with elevated SAG expression was 27.1 mo +/- 3.9 mo {[}95\% confidence interval (CI): 19.3-34.9], and in patients with reduced expression, it was 32.1 mo +/- 2.5 mo (95\% CI: 27.3-36.9). The corresponding values for Bcl-XL were 28.0 mo +/- 4.1 mo (95\% CI: 19.9-36.1) and 31.7 mo +/- 2.9 mo (95\% CI: 26.0-37.5), and those for Bak were 29.8 mo +/- 3.7 mo (95\% CI: 22.5-37.2) and 30.6 mo +/- 2.4 mo (95\% CI: 25.5-35.0), respectively. CONCLUSION: Two-year survival rates significantly correlated with low SAG expression, and SAG may be a candidate gene for good prognosis, independent of therapeutic response of different individuals. (C) 2011 Baishideng. All rights reserved.
Structural characterization of recombinant bovine Go alpha by spectroscopy and homology modeling
(IOS PRESS, 2011-01-01) Tiber, Pinar Mega; Orun, Oya; Nacar, Cevdet; Sezerman, Ugur Osman; Severcan, Feride; Severcan, Mete; Matagne, Andre; Kan, Beki
Go, a member of heterotrimeric guanine nucleotide-binding proteins, is the most abundant form of G protein in the central and peripheral nervous systems. Go alpha has a significant role in neuronal development and function but its signal transduction mechanism remains to be clarified. In this study, the bovine Go alpha subunit was overexpressed and purified into homogeneity. Its activity was studied using {[}S-35] GTP gamma S binding, intrinsic fluorescence and BODIPY assays. The secondary structure was determined by both FTIR and CD spectroscopy as 42.3\% alpha-helix, 13.4\% beta-sheet and 24.3\% beta-turn. A theoretical structure model was constructed. The structure from homology modeling is in very good agreement with the crystal structure of mouse Go alpha subunit except for the loop between alpha B-alpha C helices. This model was docked to the mouse RGS16 molecule. T117 on the alpha B-alpha C loop of Go alpha interacted with K172 on RGS16 as opposed to the T117 and K164 interaction in mouse.
Effects of carbachol on apoptosis in human chronic myelogenous leukemic K562 cell line
(MARMARA UNIV, FAC MEDICINE, 2019-01-01) Aydin, Banu; Tulunay, Aysin; Eksioglu-Demiralp, Emel; Kan, Beki; Cabadak, Hulya
Objectives: Muscarinic receptors mediate diverse actions of acetylcholine in the central nervous system and in non-nervous tissues innervated by the parasympathetic nervous system. Our study aims to evaluate the potential association of the M-3 muscarinic receptor with K562 cell proliferation and death. Materials and Methods: Cell proliferation was evaluated by bromodeoxyuridine (BrDU) incorporation. To show early, late apoptosis and cell death, cells were labelled with Annexin V, propidium iodide (PI) and analyzed by flow cytometry. Nuclear extracellular signal-regulated kinase (ERK/pERK) expression was measured by western blot analysis. Results: Treatment with carbachol (CCh) for 48h decreased cell number. Exposing K562 cells to CCh for 24h decreased the number of early apoptotic cells but did not change the number of late apoptotic and necrotic cells. CCh treatment for 48h increased the number of necrotic cells, but decreased the number of early and late apoptotic cells. In response to CCh, nuclear ERK expression was increased and this effect was reversed by 1,1-dimethyl-4-diphenylacetoxypiperidinium iodide (4DAMP). Nuclear pERK expression was decreased in CCh treated cells, 4DAMP did not reverse the effect. Conclusion: Our data suggest that cholinergic agonist CCh affects cell proliferation in K562 cells not only through muscarinic receptors but also through other cholinergic receptors.
Muscarinic agonist, antagonists and signaling pathway inhibitors change c-Fos and cyclin D-1 expression in K562 cells
(MARMARA UNIV, FAC MEDICINE, 2013-01-01) Cabadak, Hulya; Aydin, Banu; Kan, Beki
Objectives: Muscarinic acetylcholine receptors (mAChR) belong to a family of G protein coupled receptors (GPCRs). These mAChRs regulate several important physiological functions by activating a wide variety of cellular signaling pathways. We have previously shown that muscarinic acetylcholine (M-2, M-3 and M-4) receptors are expressed in K562 cells. In this study, we investigated the effect of muscarinic agonist, antagonists and different signaling pathway inhibitors on c-Fos and cyclin D-1 transcripts, using reverse transcriptase polymerase chain reaction (RT-PCR) that allows changes of very rare transcripts to be monitored. Material and Methods: Total RNA was prepared from K562 cells challenged with muscarinic agonist, antagonists and inhibitors. c-Fos and cyclin D-1 expression were determined by RT-PCR. Results: We showed that treatment with muscarinic agonist, antagonists and inhibitors leads to changes in c-Fos and cyclin D-1 expression in K562 cells. Conclusions: Our results suggest that muscarinic receptors regulate expression of c-Fos and cyclin D-1 genes in K562 cells via different signaling pathways.

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