Person: ŞAHİN, ALİ
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ŞAHİN
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ALİ
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Publication Metadata only Antitumor and antimetastatic effects of walnut oil in esophageal adenocarcinoma cells(CHURCHILL LIVINGSTONE, 2018) ŞAHİN, ALİ; Batirel, Saime; Yilmaz, Ayse Mine; Sahin, Ali; Perakakis, Nikolaos; Ozer, Nesrin Kartal; Mantzoros, Christos S.Background: Walnuts contain many components including specific fatty acids, which could be active against cancer. Even though the anticarcinogenic effect of some of the individual fatty acids in walnut oil has been described, the effect of walnut oil itself on esophageal cancer cells hasn't yet been investigated. Objective: We aimed to investigate whether walnut oil affects tumor growth and metastatic potential in esophageal cancer cells. Methods: The human esophageal adenocarcinoma cell line, OE19, was treated with different doses of walnut oil and cell viability, apoptosis/necrosis and cell cycle analyses were performed using WST-1 assay and flow cytometry respectively. Adhesion, colony formation and wound healing assays were performed to assess the antimetastatic effects of walnut oil. NFkB expression was evaluated with western blot analysis. Results: Walnut oil decreased the cell viability of esophageal cancer cells in a dose-dependent manner. 20 mg/mL walnut oil reduced cell viability by similar to 50% when compared with control. The analysis revealed that necrosis and accumulation of cells in G0/G1 phase was induced in the cells treated with high doses of walnut oil. It also down-regulated the protein levels of NFkB. Walnut oil suppressed the adhesion, migration and colony formation of the cells. Conclusions: High-dose short-term administration of walnut oil reduces the cell viability and metastatic ability of esophageal cancer cells, while exhibiting anticarcinogenic effect by inducing necrosis and cell cycle arrest at the G0/G1 phase, probably through suppression of the NFkB pathway. These data indicate that walnut oil, and by extension walnut consumption, may have beneficial effects in esophageal cancer in humans. This should be tested by clinical trials in the future. (C) 2017 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.Publication Metadata only ER stress related lipid accumulation and apoptotic cell death in nonalcoholic fatty liver diesease(ELSEVIER SCIENCE INC, 2017) ŞAHİN, ALİ; Demirel, Tugce; Sozen, Erdi; Sahin, Ali; Karademir, Betul; Ozer, Nesrin KartalPublication Metadata only Chemotherapy Resistance: The role of proteasomal degradation and heat shock response(ELSEVIER SCIENCE INC, 2015) ŞAHİN, ALİ; Karademir, Betul; Sozen, Erdi; Bozaykut, Perinur; Altundag, Ergul Mutlu; Yilmaz, Ayse Mine; Sahin, Ali; Corek, Ceyda; Sari, Gulce; Ozer, Nesrin KartalPublication Metadata only Endoplasmic reticulum stress related molecular mechanisms in nonalcoholic steatohepatitis(ELSEVIER IRELAND LTD, 2016) ŞAHİN, ALİ; Bozaykut, Perinur; Sahin, Ali; Karademir, Betul; Ozer, Nesrin KartalNonalcoholic steatohepatitis (NASH) is considered to be a common health problem since the incidence of nonalcoholic fatty liver disease (NAFLD) has increased in recent years. Disturbed hepatic cholesterol homeostasis and free cholesterol accumulation in liver results in increased oxidative stress leading to the endoplasmic reticulum (ER) stress. Activated ER stress maintains protein homeostasis however, delayed or inadequate ER stress responses may induce fat accumulation, insulin resistance, inflammation, apoptosis, and autophagy, all of which increase with age and play crucial roles in the pathogenesis of NASH. In aging research, there is a growing interest for the role of ER stress in the progression of NASH since aging seems to favor NAFLD according to its pathogenesis. On the other hand, specific microRNAs (miRNAs) expression profiles are strongly related with ER stress as well as NASH progresses. This review highlights molecular mechanisms related to ER stress in the pathogenesis of NASH and miRNAs for the progression and treatment of the disease. (C) 2016 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only alpha-Tocopherol supplementation reduces inflammation and apoptosis in high cholesterol mediated nonalcoholic steatohepatitis(WILEY, 2021) SÖZEN, AHMET ERDİ; Demirel-Yalciner, Tugce; Sozen, Erdi; Ozaltin, Esra; Sahin, Ali; Ozer, Nesrin KartalInflammation and apoptosis signaling are crucial steps in the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). Alpha-tocopherol, the most active form of vitamin E, is an important modulator of signaling mechanisms, but its involvement to cholesterol-induced NASH pathogenesis remains poorly defined. Herein we have reported a novel effect of alpha-tocopherol in the transition from hepatic steatosis to NASH. High cholesterol diet alone (without alpha-tocopherol) in rabbits elevated NASH development as indicated by increased inflammatory response, apoptotic activity and liver fibrosis. Such elevation results from induction of signaling mechanisms since the expressions of IL1 beta, phospho c-Jun/c-Jun ratio, JNK, caspase 9, CHOP and Bax were increased, and recruitment of macrophage, alpha-smooth muscle actin (alpha-SMA) and COL1A1 into the liver tissue were induced. Alpha-tocopherol supplementation inhibited inflammatory response, apoptosis and fibrosis development without affecting lipid accumulation in high cholesterol-induced NASH. Specifically, alpha-tocopherol lowered the inflammatory level as observed by reduced macrophage infiltration and JNK/c-Jun signaling. Lower inflammatory status co-occurred with the reduction of CHOP and Bax expressions as well as fibrosis-related COL1A1 and alpha-SMA levels. Taken together, alpha-tocopherol supplementation inhibits cholesterol-induced NASH development by lowering JNK/c-Jun/inflammation axis in addition to JNK/CHOP/apoptosis signaling, which might contribute to resistance against NAFLD/NASH transition.