Browsing by Author "Cincin, Zeynep Birsu"

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Citation - WoS: 59
Anti-proliferative, apoptotic and signal transduction effects of hesperidin in non-small cell lung cancer cells
(Springer, 2015) Cincin, Zeynep Birsu; Unlu, Miray; Kiran, Bayram; Bireller, Elif Sinem; Baran, Yusuf; Cakmakoglu, Bedia; Baran, Yusuf
Hesperidin, a glycoside flavonoid, is thought to act as an anti-cancer agent, since it has been found to exhibit both pro-apoptotic and anti-proliferative effects in several cancer cell types. The mechanisms underlying hesperidin-induced growth arrest and apoptosis are, however, not well understood. Here, we aimed to investigate the anti-proliferative and apoptotic effects of hesperidin on non-small cell lung cancer (NSCLC) cells and to investigate the mechanisms involved. The anti-proliferative and apoptotic effects of hesperidin on two NSCLC-derived cell lines, A549 and NCI-H358, were determined using a WST-1 colorimetric assay, a LDH cytotoxicity assay, a Cell Death Detection assay, an AnnexinV-FITC assay, a caspase-3 assay and a JC-1 assay, respectively, all in a time- and dose-dependent manner. As a control, non-cancerous MRC-5 lung fibroblasts were included. Changes in whole genome gene expression profiles were assessed using an Illumina Human HT-12v4 beadchip microarray platform, and subsequent data analyses were performed using an Illumina Genome Studio and Ingenuity Pathway Analyser (IPA). We found that after hesperidin treatment, A549 and NCI-H358 cells exhibited decreasing cell proliferation and increasing caspase-3 and other apoptosis-related activities, in conjunction with decreasing mitochondrial membrane potential activities, in a dose- and time-dependent manner. Through a GO analysis, by which changes in gene expression profiles were compared, we found that the FGF and NF-kappa B signal transduction pathways were most significantly affected in the hesperidin treated NCI-H358 and A549 NSCLC cells. Our results indicate that hesperidin elicits an in vitro growth inhibitory effect on NSCLC cells by modulating immune response-related pathways that affect apoptosis. When confirmed in vivo, hesperidin may serve as a novel anti-proliferative agent for non-small cell lung cancer.
Citation - WoS: 32
Apoptotic Effects of Quercitrin on DLD-1 Colon Cancer Cell Line
(Frontiers Media Sa, 2015) Cincin, Zeynep Birsu; Unlu, Miray; Kiran, Bayram; Bireller, Elif Sinem; Baran, Yusuf; Cakmakoglu, Bedia; Baran, Yusuf
Quercetin, which is the most abundant bioflavonoid compound, is mainly present in the glycoside form of quercitrin. Although different studies indicated that quercitrin is a potent antioxidant, the action of this compound is not well understood. In this study, we investigated whether quercitrin has apoptotic and antiproliferative effects in DLD-1 colon cancer cell lines. Time and dose dependent antiproliferative and apoptotic effects of quercitrin were subsequently determined by WST-1 cell proliferation assay, lactate dehydrogenase (LDH) cytotoxicity assay, detection of nucleosome enrichment factor, changes in caspase-3 activity, loss of mitochondrial membrane potential (MMP) and also the localization of phosphatidylserine (PS) in the plasma membrane. There were significant increases in caspase-3 activity, loss of MMP, and increases in the apoptotic cell population in response to quercitrin in DLD-1 colon cancer cells in a time- and dose-dependent manner. These results revealed that quercitrin has antiproliferative and apoptotic effects on colon cancer cells. Quercitrin activity supported with in vivo analyses could be a biomarker candicate for early colorectal carcinoma.
Citation - WoS: 0
EFFECTS OF HESPERIDIN ON NON-SMALL CELL LUNG CANCER CELLS
(int inst Anticancer Research, 2014) Bireller, Elif Sinem; Cincin, Zeynep Birsu; Unlu, Miray; Kiran, Bayram; Baran, Yusuf; Cakmakoglu, Bedia; Baran, Yusuf
[No Abstract Available]
Citation - WoS: 1
Investigation of Potential Anticarcinogenic Effects of Corilagin in Lung Cancer Cells
(Marmara Univ, inst Health Sciences, 2019) Rencuzogullari, Cagla; Cincin, Zeynep Birsu; Iplik, Elif Sinem; Baran, Yusuf; Cakmakoglu, Bedia; Baran, Yusuf
Objective: Lung cancer (LC) is the most extensive reason of cancer associated deaths in men and women in the world. LC categorizes into two main groups due to their molecular clinicopathological features and therapeutic responses. Non-small cell lung cancer (NSCLC) is the main subgroup that consists of nearly 85% of all lung cancer types. Corilagin, a biologically active ellagitannin, could be extracted from Phyllanthus species which are known as Chinese medicinal plant. It has been recently shown that Corilagin could exert anti-inflammatuar and antioxidative effects in different experimental cancer models. However, the molecular effects of Corilagin in NSCLC remain unclear. Methods: In this study, the antiproliferative and apoptotic effects of Corilagin were identified by WST-1 cell proliferation test, caspase-3 and mitochondrial membrane potential (MMP). Results: We found that Corilagin significiantly suppressed the proliferation of NSCLC cells. Furthermore, we also showed that Corilagin could contribute apoptosis by inducing activity of caspase-3 molecule and loss of MMP. Conclusion: Taken together, our study first showed that Corilagin could be a new treatment method for NSCLC after verifying its effects with in vivo and clinical studies.
Citation - WoS: 54
Molecular Mechanisms of Quercitrin-induced Apoptosis in Non-small Cell Lung Cancer
(Elsevier Science inc, 2014) Cincin, Zeynep Birsu; Unlu, Miray; Kiran, Bayram; Bireller, Elif Sinem; Baran, Yusuf; Cakmakoglu, Bedia; Baran, Yusuf
Background and Aims. Quercitrin (QR; quercetin-3-0-rhamnoside) has been used previously as an antibacterial agent and has been shown to inhibit the oxidation of low-density lipoproteins and prevent an allergic reaction. Furthermore, it was demonstrated that quercitrin exerts protective effects against H2O2-induced dysfunction in lung fibroblast cells. However, the mechanisms of quercitrin effects on cancer cell proliferation and apoptosis is not well understood. The aim of this study is to investigate the cytotoxic and apoptotic effects of quercitrin and the molecular mechanisms of quercitrin-induced apoptosis in non-small cell lung cancer (NSCLC) cell lines. Methods. Time- and dose-dependent antiproliferative and apoptotic effects of quercitrin determined by WST-1 cell proliferation assay, lactate dehydrogenase (LDH) cytotoxicity assay, determination of nucleosome enrichment factor, changes in caspase-3 activity, loss of mitochondrial membrane potential (MMP) and also the localization of phosphatidylserine in the plasma membrane. Changes in whole genome gene expression levels were examined by Illumina Human HT-12v4 beadchip microarrays. Results. There were significant increases in caspase-3 activity, loss of MMP, and increases in apoptotic cell population in response to quercitrin in A549 and NCI-H358 NSCLC cells in a time- and dose-dependent manner. Conclusion. Our results demonstrated that genes involved in leukocyte transendothelial migration, cell adhesion and phosphatidylinositol signaling system pathways were the most statistically significant pathways in NCI-H358 and A549 cells. These results revealed that quercitrin has antiproliferative and apoptotic effects on lung cancer cells by modulating the immune response. After confirming its anticarcinogenic effects in vivo, quercitrin could be a novel and strong anticancer agent against NSCLC. (C) 2014 IMSS. Published by Elsevier Inc.
Citation - WoS: 27
New indication for therapeutic potential of an old well-known drug (propranolol) for multiple myeloma
(Springer, 2013) Kozanoglu, Ilknur; Yandim, Melis Kartal; Cincin, Zeynep Birsu; Ozdogu, Hakan; Cakmakoglu, Bedia; Baran, Yusuf; Baran, Yusuf
Propranolol, a non-selective beta-adrenergic receptor blocker, has been used for the treatment of the patients with hypertension for more than 50 years. There are several in vitro and in vivo evidences that beta-adrenergic receptor antagonists inhibit proliferation and angiogenesis and also increase apoptosis in breast, skin, and colon cancers. The aim of this study was to investigate the cytotoxic and apoptotic effects of propranolol and the genes involved in propranolol-induced apoptosis in multiple myeloma cells. Time-dependent antiproliferation and apoptotic effects of propranolol were subsequently determined by MTT cell proliferation assay, changes in caspase-3 activity, loss of mitochondrial membrane potential (MMP), and also the localization of phosphatidylserine in the plasma membrane. Changes in expression levels of NF-IeB pathway were examined by qRT-PCR array. IC50 values of propranolol on U266 cells were calculated as 141, 100, and 75 mu M after 24-, 48-, and 72-h propranolol exposure, respectively. There were significant increases in caspase-3 activity, loss of MMP, and increases in apoptotic cell population in response to propranolol in U266 cells in a time- and dose-dependent manner. There were increases in expression levels of BCL10, TRAF family members, interleukins, TLR1-4, TNFRSF10B, NF-kappa B, and the inhibitors of NF-kappa B genes, and significant decreases in expression levels of Bcl-2 in response to propranolol treatment were observed. These results revealed that propranolol has antiproliferative and apoptotic effects on multiple myeloma cells. Being supported with in vivo analyses, propranolol can be a good and economical way to treat multiple myeloma patients.