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YALÇIN, AHMET SUHA

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YALÇIN

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AHMET SUHA

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2016 - 20203
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Author: YILMAZ, BETÜL × Start date: 2000 ×

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Now showing 1 - 3 of 3
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    Redox Regulation and Cancer Therapy
    (BENTHAM SCIENCE PUBL LTD, 2018) YALÇIN, AHMET SUHA; Yalcin, A. Suha; Karademir, Betul
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    The potential use of natural products to negate hepatic, renal and neuronal toxicity induced by cancer therapeutics
    (PERGAMON-ELSEVIER SCIENCE LTD, 2020) YALÇIN, AHMET SUHA; Prsa, Patrik; Karademir, Betul; Bicim, Gokhan; Mahmoud, Hatem; Dahan, Inbal; Yalcin, A. Suha; Mahajna, Jamal; Milisav, Irina
    Different types of chemotherapeutics are used for cancer treatment. These drugs act on several signal pathways, lead to programmed cell death, and damage cancer cells. Although many specific mechanisms of action have been suggested for chemotherapeutics, there are still gaps in understanding their effects. They may affect different components of the cell, particularly proteins with specific functions, such as enzymes. Recently, targeted and immuno therapies were introduced for treatment of different cancers. However, many cancer patients still depend on traditional and well-known drugs. Doxorubicin and platinum-based drugs are among the most frequently used chemotherapeutics. They are highly cytotoxic for cancer cells, but they also act on healthy cells. Hence, it is crucial to understand the mechanisms involved in order to decrease their side effects. Natural products, many of which are also available over-the-counter, may be considered to decrease various cancer drug-induced side effects. This review focuses on the use of these compounds to overcome side effects of chemotherapeutics, primarily doxorubicin and cisplatin, in the liver, kidney, and neuronal systems.
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    Quercetin-Induced Cell Death in Human Papillary Thyroid Cancer (B-CPAP) Cells
    (HINDAWI LTD, 2016) YALÇIN, AHMET SUHA; Altundag, Ergul Mutlu; Kasaci, Tolga; Yilmaz, Ayse Mine; Karademir, Betul; Kocturk, Semra; Taga, Yavuz; Yalcin, A. Suha
    In this study, we have investigated the antiproliferative effect of quercetin on human papillary thyroid cancer cells and determined the apoptotic mechanisms underlying its actions. We have used different concentrations of quercetin to induce apoptosis and measured cell viability. Apoptosis and cell cycle analysis was determined by flow cytometry using Annexin V and propidium iodide. Finally, we have measured changes in caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels as hallmarks of apoptosis and Hsp90 protein expression level as a marker of proteasome activity in treated and control cells. Quercetin treatment of human papillary thyroid cancer cells resulted in decreased cell proliferation and increased rate of apoptosis by caspase activation. Furthermore, it was demonstrated that quercetin induces cancer cell apoptosis by downregulating the levels of Hsp90. In conclusion, we have shown that quercetin induces downregulation of Hsp90 expression that may be involved in the decrease of chymotrypsin-like proteasome activity which, in order, induces inhibition of growth and causes cell death in thyroid cancer cells. Thus, quercetin appears to be a promising candidate drug for Hsp90 downregulation and apoptosis of thyroid cancer cells.