Browsing by Author "Akar, Sakine"

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A Benzimidazolium Salt Induces Apoptosis and Arrests Cells at Sub-G1 Phase in Epithelial Ovarian Cancer Cells
(Springer, 2024) Akar, Sakine; Cakir, Mustafa; Ozkol, Halil; Akkoc, Senem; Ozdem, Berna
BackgroundOvarian cancer, also known as a silent killer, is the deadliest gynecological cancer in women worldwide. Epithelial ovarian cancers constitute the majority of ovarian cancers, and diagnosis can be made in advanced stages, which greatly reduces the likelihood of treatment and lowers the survival rate. For the treatment of epithelial ovarian cancers, the search for synthetic agents as well as agents of natural origin continues. The effects of 1-(2-cyanobenzyl)-3-(4-vinylbenzyl)-1H-benzo[d]imidazole-3-ium chloride (BD), a benzimidazole derivative, were investigated on epithelial ovarian cancer cells.Methods and resultsIn our study, the effects of BD on proliferation, colony formation, cell death by apoptosis and the cell cycle in A2780 and A2780 Adriamycin (ADR) ovarian cancer cell lines were investigated. Proliferation was examined with cell viability analysis, colony formation and apoptosis with Annexin V staining and cell cycle analyses with PI staining, respectively. As a result of the analyses, BD inhibited cell proliferation and colony formation, induced apoptosis and cell death at 48 h in A2780 and A2780 ADR cells at 10.10 and 10.36 mu M concentrations, respectively. In addition, A2780 and A2780ADR cells were arrested in the Sub-G1 phase of the cell cycle.ConclusionsBD suppresses cancer cell progression by showing antiproliferative effects on ovarian cancer cells. Further analyses are required to determine the mechanism of action of this agent and to demonstrate its potential as a suitable candidate for the treatment of epithelial ovarian cancer.
A Benzimidazolium Salt Induces Apoptosis and Arrests Cells at Sub-G1 Phase in Epithelial Ovarian Cancer Cells (Vol 51, 66, 2024)
(Springer, 2024) Akar, Sakine; Cakir, Mustafa; Ozkol, Halil; Akkoc, Senem; Ozdem, Berna
Downregulation of Glutaminase 1 (Gls1) Inhibits Proliferation, Clonogenicity, and Migration of Aggressive Mda-Mb Breast Cancer Cells by Increasing P21 and Decreasing Integrin-Β1 Expression
(Erciyes Univ Sch Medicine, 2022) Akar, Sakine; Donmez-Altuntas, Hamiyet; Hamurcu, Zuhal
Objective: Glutamine metabolism is an important pathway in cell proliferation and tumor progression. The first enzyme to be converted in the process of glutamine metabolism, glutaminase 1 (GLS1), exhibits increased expression in many types of cancer, including breast cancer. Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with high glutamine metabolic activity. The aim of this research was to examine the effects on glutamine metabolism and carcinogenic properties following small interfering RNA (siRNA)-mediated inhibition of GLS1 in glutamine-dependent TNBC.Materials and Methods: The effects on cell proliferation, migration, apoptosis, colony formation, and the cell cycle of MDA-MB-231 cells using different siRNAs targeting GLS1 were analyzed using an MTS assay, a wound-healing assay, clo-nogenic analysis, and annexin V and propidium iodide staining methods. The protein expression of GLS1, integrin beta 1 (beta 1), caspase-3, and p21 were examined using western blot analysis and flow cytometry.Results: The findings revealed that cell viability, migration, and colony formation were significantly suppressed in MDA-MB-231 cells transfected with 2 different GLS1 siRNAs. Furthermore, the results of flow cytometry and western blot analysis demonstrated that knockdown of GLS1 induced arrest in the G0/G1 phase of the cell cycle through the p21 signaling pathway, but did not induce apoptosis.Conclusion: GLS1 is needed for cell proliferation and promotes tumor progression and growth of MDA-MB 231 cells. siRNAs may provide a means to downregulate GLS1 and offer a promising target for breast cancer therapy.
The Effects of Oral Supplementation of Carvacrol on Autophagy and Epithelial To Mesenchymal Transition Regulation in Uv-Induced Skin Damage
(Taylor & Francis Ltd, 2025) Alvur, Ozge; Ozkol, Halil; Altindag, Fikret; Ozkol, Hatice Uce; Evyapan, Gulsah; Akar, Sakine
ObjectiveThe skin is the biggest organ of the body being most exposed to UV radiation (UVR). Many skin diseases may develop due to UV exposure. Thus, it is extremely important to reveal molecules that can prevent these diseases.Material and methodCarvacrol (CVC), a liquid phenolic monoterpenoid is found in thyme and some plants related to thyme. In our study, for the first time in the literature we aimed to determine the effects of CVC on autophagy and Epithelial to Mesenchymal Transition (EMT) mechanisms in skin damage of rats exposed to combined UVA and UVB radiation. For this purpose, twenty-eight rats were divided into four groups: I (Control), II (CVC alone), III (UVA + UVB), IV (UVA + UVB + CVC). While UVA + UVB was applied without any treatment in Group III, this application was performed with CVC support in Group IV. As for the animals in Group II, only carvacrol was given. On the 30th day of the trial, expression of certain genes playing a role in autophagy and EMT pathways were evaluated at mRNA and protein level by qRT-PCR and immunohistochemical staining in the shaved back skin tissues of rats.ResultsBased on our results, it can be concluded that CVC may prevent autophagic cell death by suppressing autophagy and it might support the wound healing process by inducing EMT in UV-induced skin damage. The molecular mechanisms of the effect of CVC on autophagy and EMT mechanisms should be clarified in further studies.
The Preventive Effects of Natural Plant Compound Carvacrol Against Combined Uva and Uvb-Induced Endoplasmic Reticulum Stress in Skin Damage of Rats
(Springernature, 2024) Evyapan, Gulsah; Ozkol, Halil; Ozkol, Hatice Uce; Alvur, Ozge; Akar, Sakine
The skin is constantly exposed to a variety of environmental stressors, including ultraviolet (UV) radiation. Exposure of the skin to UV radiation causes a number of detrimental biological damages such as endoplasmic reticulum (ER) stress. The ER stress response is a cytoprotective mechanism that maintains homeostasis of the ER by increasing the capacity of the ER against the accumulation of unfolded proteins in the ER. Carvacrol (CRV) is a monoterpenoid phenol found in essential oils with antimicrobial and anti-inflammatory activities. We investigated for the first time in the literature the potential protective role of CRV against combined UVA and UVB-induced skin damage by targeting the ER stress pathway in a rat model. For this purpose, expressions of Grp78, Perk, Atf6, Ire-1, Chop, Xbp1, Casp12, elF2 alpha, and Traf2 genes related to ER stress were analyzed by RT-PCR and protein expression levels of GRP78, ATF6, CHOP, and XBP1 were determined by ELISA assay in tissue sections taken from the back of the rats. As a result of analysis, it was seen that the expression levels of aforementioned ER stress genes increased significantly in the UVA + UVB irradiated group compared to the control group, while their expression levels decreased markedly by supplementation of CRV in UVA + UVB + CRV group. With regard to expressions of foregoing proteins, their levels escalated notably with UVA + UVB application and decreased markedly by CRV supplementation. In conclusion, present study revealed that CRV ameliorates UVA + UVB-induced ER stress via reducing the expression of mRNA as well as proteins involved in the unfolded protein response (UPR) pathway and inducing apoptosis as evidenced from high Caspase12 level.
Β-Escin Reduces Cancer Progression in Aggressive Mda-Mb Cells by Inhibiting Glutamine Metabolism Through Downregulation of C-Myc Oncogene
(Springer, 2022) Akar, Sakine; Donmez-Altuntas, Hamiyet; Hamurcu, Zuhal
Background The c-myc oncogene, which causes glutamine dependence in triple negative breast cancers (TNBC), is also the target of one of the signaling pathways affected by beta-Escin. Methods and results We sought to determine how c-myc protein affects glutamine metabolism and the proteins, glutamine transporter alanine-serine-cysteine 2 (ASCT2) and glutaminase (GLS1), in beta-Escin-treated MDA-MB-231 cells using glutamine uptake and western blot analysis. Cell viability, colony formation, migration and apoptosis were also evaluated in MDA-MB-231 cells in response to beta-Escin treatment using MTS, colony forming, wound healing, and Annexin-V assay. We determined that beta-Escin decreased glutamine uptake and reduced c-myc and GLS1 protein expressions and increased the expression of ASCT2. In addition, this inhibition of glutamine metabolism decreased cell proliferation, colony formation and migration, and induced apoptosis. Conclusions In this study, it was suggested that beta-Escin inhibits glutamine metabolism via c-myc in MDA-MB-231 cells, and it is thought that as a result of interrupting the energy supply in these cells via c-myc, it results in a decrease in the carcinogenic properties of the cells. Consequently, beta-Escin may be promising as a therapeutic agent for glutamine-dependent cancers.