Scopus İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12573/395
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Book Part Pleiotropic Molecular Effects of Dietary Polyphenols Resveratrol and Apigenin in Leukemia(Elsevier, 2018) Adan, Aysun; Oğuz, OsmanResveratrol and apigenin are commonly found polyphenols in many fruits and vegetables and recognition of these dietary polyphenols for human health owing to their biological and pharmacological features including antiinflammatory and antioxidative functions has increased recently. In addition to direct antioxidative effects, they have impacts on various important signaling pathways dysregulated in cancer, genetic and epigenetic regulators, transcription factors and even on miRNAs as anticarcinogenic compounds. Numerous in vitro and in vivo studies have demonstrated their pleiotropic molecular mechanisms of action in cancer, particularly in solid tumors. However, in recent years, significant progress has been made in studying the antileukemic effects of resveratrol and apigenin at the cellular and molecular levels. Herein, we have critically discussed the main molecular targets of resveratrol and apigenin and their promising potential as chemopreventive agents as well as their limitations, with a special emphasis on leukemias. © 2021 Elsevier B.V., All rights reserved.Article Efficacy of Combinatorial Inhibition of Hedgehog and Autophagy Pathways on the Survival of AML Cell Lines(Academic Press inc Elsevier Science, 2025-08) Sansacar, Merve; Pepe, Nihan Aktas; Akcok, Emel Basak Gencer; El Khatib, Mona; Gencer Akçok, Emel BaşakAcute myeloid leukemia (AML) is a common hematopoietic disease that results from diverse genetic abnormalities. Dysregulation of important signaling pathways, including the PI3K/AKT/mTOR, Wnt and Hedgehog pathways, plays crucial roles in the development of AML. Hedgehog pathway (Hh) is a conserved signaling pathway that is crucial throughout embryogenesis. Hh plays an important role in the regulation of autophagy, known as the cellular recycling process of organelles and unwanted proteins. Many studies have noted that the modulation of autophagy could act as a survival mechanism in AML. Considering the pivotal role of autophagy and Hh signaling in AML, understanding the relationship between these pathways is important for overcoming leukemia. Therefore, we examined the efficacy of Hh inhibition by GLI-ANTagonist 61 (GANT61) in MOLM-13 and CMK cells via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenil-2H-tetrazolium bromide (MTT) cell viability assays. GANT61 resulted in decreased cell viability in both cell lines. Therefore, we focused on the outcome of autophagy modulation in AML cells. We observed that the autophagy inhibitors ammonium chloride (NH4CI), chloroquine (CQ), and nocodazole led to a significant reduction in the proliferation of both cell lines. Cotreatment with autophagy pathway inhibitors and GANT61 synergistically affected both AML cell lines. Moreover, dual targeting of these pathways resulted in arrest at the G0/G1 phase in MOLM-13 cells but not in CMK cells. Furthermore, the combination of nocodazole and GANT61 increased the expression level of LC3B-II in both cell lines. Compared with that in the untreated control cells, the GLI1 gene expression level in both cell lines was significantly lower after GANT61 and autophagy cotreatment. In conclusion, targeting Hh and autophagy could be a favorable option to combat AML.