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YILMAZ, VEYSEL TURAN

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YILMAZ

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VEYSEL TURAN

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2019 - 201922020 - 20211
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    Publication
    Unfolded protein response is involved in trans-platinum (ii) complex-induced apoptosis in prostate cancer cells via ros accumulation
    (Bentham Science Publ Ltd, 2019-01-01) Karakaş, Didem; Cevatemre, Buse; Oral, Arzu Y.; YILMAZTEPE ORAL, ARZU; Yılmaz, Veysel T.; YILMAZ, VEYSEL TURAN; Ulukaya, Engin; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.; Bursa Uludağ Üniversitesi/Fen Edebiyat Fakültesi/Kimya Bölümü.; 0000-0002-3781-6834; 0000-0002-8962-9758; 0000-0002-2849-3332; AHD-2050-2022; KMA-2321-2024; A-5841-2017; L-7238-2018; L-6682-2018
    Background: Prostate cancer is one of the most common cancer types and it is the sixth leading cause of cancer-related death in men worldwide. Even though novel treatment modalities have been developed, it still a lifethreatening disease. Therefore novel compounds are needed to improve the overall survival.Methods: In our study, it was aimed to evaluate the anti-cancer activity of newly synthesized Platinum (II) [Pt(II)] complex on DU145, LNCaP and PC-3 prostate cancer cell lines. The cytotoxic activity of Pt(II) complex was tested by SRB and ATP cell viability assays. To detect the mode of cell death; fluorescent staining, flow cytometry and western blot analyses were performed.Results: The Pt(II) complex treatment resulted in a decrease in cell viability and increasing levels of apoptotic markers (pyknotic nuclei, annexin-V, caspase 3/7 activity) and a decrease in mitochondrial membrane potential in a dose dependent manner. Among cell types, tested PC-3 cells were found to be more sensitive to Pt(II) complex, demonstrating elevation of DNA damage in this cell line. In addition, Pt(II) complex induced Endoplasmic Reticulum (ER) stress by triggering ROS generation. More importantly, pre-treatment with NAC alleviated Pt(II) complex-mediated ER stress and cell death in PC-3.Conclusion: These findings suggest an upstream role of ROS production in Pt(II) complex-induced ER stressmediated apoptotic cell death. Considering the ROS-mediated apoptosis inducing the effect of Pt(II) complex, it warrants further evaluation as a novel metal-containing anticancer drug candidate.
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    Publication
    Combination of histone deacetylase inhibitor with cu(ii) 5,5-diethylbarbiturate complex induces apoptosis in breast cancer stem cells: A promising novel approach
    (Bentham Science, 2021-01-01) Erkisa, Merve; Aztopal, Nazlihan; Erturk, Elif; Ulukaya, Engin; Yilmaz, Veysel T.; Ari, Ferda; Erkisa, Merve; Aztopal, Nazlihan; YILMAZ, VEYSEL TURAN; Ari, Ferda; ARI, FERDA; ertürk; Bursa Uludağ Üniversitesi/Fen Edebiyat Fakültesi.; 0000-0002-3127-742X; 0000-0003-3118-8061; 0000-0002-2849-3332; 0000-0002-6729-7908; JQI-3400-2023; AAM-1001-2020; L-7238-2018; AAG-7012-2021; L-6687-2018
    Background: Cancer Stem Cells (CSCs) are a subpopulation within the tumor that play a role in the initiation, progression, recurrence, resistance to drugs and metastasis of cancer. It is well known that epigenetic changes lead to tumor formation in cancer stem cells and show drug resistance. Epigenetic modulators and /or their combination with different agents have been used in cancer therapy.Objective: In our study, we scope out the effects of a combination of a histone deacetylases inhibitor, Valproic Acid (VPA), and Cu(II) complex [Cu(barb-kappa N)( barb-kappa 2N,O)(phen-kappa N,N')]center dot H2O] on cytotoxicity/apoptosis in a stem-cell enriched population (MCF-7s) obtained from parental breast cancer cell line (MCF-7).Methods: The viability of the cells was measured by the ATP assay. Apoptosis was elucidated via the assessment of caspase-cleaved cytokeratin 18 (M30 ELISA) and a group of flow cytometry analysis (caspase 3/7 activity, phosphatidylserine translocation by annexin V-FITC assay, DNA damage and oxidative stress) and 2',7'-dichlorofluorescein diacetate staining.Results: The VPA combined with Cu(II) complex showed anti-proliferative activity on MCF-7s cells in a dose-and time-dependent manner. Treatment with a combination of 2.5 mM VPA and 3.12 mu M Cu(II) complex induced oxidative stress in a time-dependent manner, as well as apoptosis evidenced by the increase in caspase 3/7 activity, positive annexin-V-FITC, and increase in M30 levels.Conclusion: The results suggest that the combination therapy induces apoptosis following increased oxidative stress, thereby making it a possible promising therapeutic strategy for which further analysis is required.
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    Publication
    Cytotoxic platinum(II) complexes derived from saccharinate and phosphine ligands: synthesis, structures, DNA cleavage, and oxidative stress-induced apoptosis
    (Springer, 2019-10-26) İçsel, Ceyda; Yılmaz, Veysel T.; Cevatemre, Buse; Aygün, Muhittin; Ulukaya, Engin; İÇSEL YILMAZ, CEYDA; YILMAZ, VEYSEL TURAN; Bursa Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Kimya Bölümü.; 0000-0002-2849-3332; L-7238-2018; AAI-3342-2021
    A series of the structurally related platinum(II) saccharinate (sac) complexes with alkylphenylphosphines, namely cis-[Pt(sac)(2)(PPh2Me)(2)]center dot DMSO (1), cis-[Pt(sac)(2)(PPhMe2)(2)] (2), cis-[Pt(sac)(2)(PPh2Et)(2)] (3), and cis-[Pt(sac)(2)(PPhEt2)(2)]center dot 2DMSO (4), were synthesized and fully characterized; their structures were determined by X-ray crystallography. All the complexes were investigated for their anticancer potentials on three human cancer cells including A549 (lung), MCF-7 (breast), and HCT116 (colon) in addition to a noncancerous human bronchial epithelial cells (BEAS-2B). Specifically, 1 and 3 showed significant cytotoxic effects against MCF-7 and HCT116 cell lines in comparison to cisplatin, and were considered as the most potent ones in the series. The cytotoxic complexes were found to cleave DNA efficiently. In addition, the binding interactions of the complexes with DNA were confirmed by enzyme inhibition and molecular docking studies. Complexes 1 and 3 were capable of inducing apoptosis and arrested the cell cycle at the DNA synthesis (S) phase in MCF-7 cells. Furthermore, 1 and 3 caused the excessive generation of reactive oxygen species (ROS), leading to mitochondrial dysfunction and double-strand DNA breaks.