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    Effects of different glucose concentrations on the leptin signaling pathway in MCF-7 and T47D breast cancer cells
    (2019) Demirel, Pınar Buket; Cleary, Margot; Tuna, Bilge Güvenç; Özorhan, Ümit; Doğan, Soner
    Aim: Leptin activates multiple intracellular signaling pathways, including JAK/STAT, by binding to its receptor. Leptin is also animportant regulator of glucose homeostasis. Although both glucose and leptin increase breast cancer cell proliferation in vitro,whether the enhancing effect of glucose on the proliferation of breast cancer cells is mediated by the leptin signaling pathway isnot known. The aim of this study was to investigate the effect of different glucose concentrations on the leptin signaling pathway inMCF-7 and T47D breast cancer cells.Material and Methods: MCF-7 and T47D cell proliferation in different glucose concentrations (2.5 mM, 5 mM, 25 mM, or 50 mM)were assayed using CCK-8 assay. Leptin, leptin receptors (ObR, ObRb) as well as STAT3 mRNA and protein levels in both cell lines indifferent glucose concentrations were examined by RT-PCR and western blot, respectively.Results: Incubation in 2.5 mM, 5 mM, 25 mM, or 50 mM glucose for 72h significantly increased the proliferation of both MCF-7 andT47D cells compared to 0 mM glucose incubated cells (P<0.001). mRNA levels of leptin, ObR, ObRb or STAT3 in 2.5 mM, 5 mM,25 mM, or 50 mM glucose incubated cells were not significantly different in both cell lines compared to 0 mM (p>0.05). However,ObR protein levels in MCF-7 cells incubated in 25 mM glucose was significantly lower compared to 0 mM glucose by western blot(p<0.05).Conclusion:Our data suggest that the enhancing effect of glucose on breast cancer cell proliferation is not mediated by the JAK/STAT pathway.
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    Noncoding RNAs in age-related cardiovascular diseases
    (Elsevier, 2022) Jusic, Amela; Thomas, Pınar Buket; Wettinger, Stephanie Bezzina; Doğan, Soner; Farrugia, Rosienne; Gaetano, Carlo; Tuna, Bilge Güvenç; Pinet, Florence; Robinson, Emma L.; Chalot, Simon Tual; Stellos, Konstantinos; Devaux, Yvan; Thomas, Pınar Buket
    Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality in the adult population worldwide and represent a severe economic burden and public health concern. The majority of human genes do not code for proteins. However, noncoding transcripts play important roles in ageing that significantly increases the risk for CVDs. Noncoding RNAs (ncRNAs) are critical regulators of multiple biological processes related to ageing such as oxidative stress, mitochondrial dysfunction and chronic inflammation. NcRNAs are also involved in pathophysiological developments within the cardiovascular system including arrhythmias, cardiac hypertrophy, fibrosis, myocardial infarction and heart failure. In this review article, we cover the roles of ncRNAs in cardiovascular ageing and disease as well as their potential therapeutic applications in CVDs.