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A PLK1 inhibitor, RO3280, suppresses proliferation of SNU-16 gastric cancer cells via apoptosis
(Bangladesh Pharmacological Soc, 2024) Yulak, Fatih; Keskin, Zekeriya
This study examines the anti -tumor, pro-apoptotic, and genotoxic effects of polo -like kinase 1 (PLK1) inhibitor RO3280 on the gastric cancer cell line SNU16. Using the XTT assay, the antiproliferative effect of the compound was identified and showed a significant antiproliferative effect (p<0.01) with the IC50 value of 9.64 M for 24 hours. RO3280 considerably enhanced the expression of Bax and cleaved caspase-3 (p<0.01) and dramatically lowered the BCL-2 level (p<0.01), demonstrating an apoptotic effect. It greatly raised the expression of 8-oxo-dG, a DNA damage marker, and cleaved PARP, a degraded version of the PARP enzyme involved in DNA repair (p<0.05 and p<0.01, respectively). In addition, flow cytometric studies for annexin V and caspase3/7 revealed that RO3280 markedly improved the apoptotic cell profile (p<0.01). It reduced the mitochondrial membrane potential and DNA damage (p<0.01). These findings suggest that RO3280 has an antitumor impact by damaging DNA and inducing apoptosis in SNU-16 gastric cancer cells.
Anticancer activity of sinapic acid by inducing apoptosis in HT-29 human colon cancer cell line
(Canadian Science Publishing, 2023) Tastemur, Seyma; Hacisuleyman, Levent; Karata, Ozhan; Yulak, Fatih; Ataseven, Hilmi
Colorectal cancer is the third most lethal and fourth most commonly diagnosed cancer worldwide. Sinapic acid, a derivative of hydroxycinnamic acid, is a promising phytochemical exhibiting numerous pharmacological activities in various systems. It is a substantial chain-breaking antioxidant that operates as a radical scavenger. The aim of this research was to investigate the antiproliferative effect of sinapic acid on the HT-29 cell line besides the mechanisms underlying this activity. The effect of sinapic acid on the viability of HT-29 cell line was investigated using XTT assay. The levels of BCL-2, cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG were measured using ELISA. Gamma-H2AX and cytochrome c expressions were assessed semiquantitatively using immunofluorescence staining. Sinapic acid at 200 & mu;m and higher doses produced a significant antiproliferative effect on HT-29 cells. The IC50 value was found to be 317.5 & mu;m for 24 h. Sinapic acid (317.5 & mu;m) significantly elevated cleaved caspase 3, BAX, cleaved PARP, and 8-oxo-dG levels. The levels of gamma-H2AX foci are significantly higher, while the levels of cytochrome c are lower in sinapic acid-treated HT-29 cells. These results indicate that sinapic acid has antiproliferative, apoptotic, and genotoxic effects on colon cancer cells.
Death receptor-dependent apoptosis and cell cycle delay induced by bioymifi in human cervical cancer cells
(Univ Karachi, 2022) Altun, Ahmet; Inan, Zeynep Deniz Sahin; Yulak, Fatih
In chemotherapy applied against cervical cancer, non-specific cytotoxicity and drug resistance that develops over time are trying to be overcome. Therefore, the development of effective and innovative chemotherapeutic drugs for the treatment is among the priority issues in the medical field. The anticancer activity of the Bioymifi, which can activate apoptosis by inducing DR-5 clustering and aggregation against the human cervical cancer cell line, was investigated in the current study. The cytotoxic activity of Bioymifi on the HeLa cell line was identified using XTT assay. The pathway of the cell death mechanism was analyzed through the cell cycle and Annexin V assays by the flow cytometry. DAPI staining assay was applied under fluorescence microscopy to examine the nuclear morphology. Bioymifi appeared to have a remarkable IC50 value (11.75??M) against HeLa cells. The cell cycle analysis demonstrated the increase of Bioymifi cured HeLa cells in the S phase. And also, 11.75??M of Bioymifi caused a significantly higher apoptotic effect compared to control. In addition, in vitro immunofluorescence experiments of this study represented that Bioymifi reduced Ki-67 localization in HeLa cells. Bioymifi has significantly anticancer actions in Human cervix cancer in vitro and can be combined with standard treatment.
Enoxaparin Protects C6 Glioma Cells from Glutamate-Induced Cytotoxicity by Reducing Oxidative Stress and Apoptosis
(Springer, 2025) Yulak, Fatih; Joha, Ziad; Ozturk, Aysegul; Inan, Zeynep Deniz Sahin; Taskiran, Ahmet Sevki
Recent studies suggest enoxaparin may protect the central nervous system (CNS) from damage. However, its specific effects on glial cells and the underlying mechanisms involving cell death and oxidative stress require further investigation. Therefore, this research investigated enoxaparin's potential to safeguard C6 glioma cells against glutamate-induced cytotoxicity, specifically focusing on its influence on oxidative stress and apoptotic mechanisms. To investigate the neuroprotective effects of enoxaparin against glutamate-induced cytotoxicity in C6 cells, four groups were established: a control group, a group exposed to 10 mM glutamate, a group treated with enoxaparin at concentrations ranging from 25 to 200 mu M, and a group receiving both 10 mM glutamate and enoxaparin at concentrations ranging from 25 to 200 mu M. Cell viability was measured using an XTT assay. To evaluate the effects of enoxaparin on oxidative stress, superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured using ELISA, along with total antioxidant status (TAS) and total oxidant status (TOS). Apoptosis was evaluated using flow cytometry, and caspase-3 activity, a key marker of apoptosis, was assessed using caspase-3 immunofluorescence staining. Enoxaparin at 50, 100, and 200 mu M markedly increased cell viability in the enoxaparin + glutamate group. Enoxaparin treatment in the enoxaparin + glutamate group also significantly elevated levels of SOD and TAS, while concurrently decreasing MDA and TOS levels. These changes indicate a reduction in oxidative stress. Enoxaparin treatment further resulted in a significant decline in cleaved caspase-3 levels, a marker of apoptosis. Enoxaparin pre-treatment reduced cell death according to flow cytometry analysis. This study suggests enoxaparin's potential to shield C6 glioma cells from glutamate-induced cell death by mitigating both oxidative stress and apoptotic pathways. More research is needed to confirm this effect.
ETP 45658’in ht-29 kolon kanseri hücrelerine karşı antiproliferatif etkisinin altında yatan moleküler mekanizmaların araştırılması
(Sivas Cumhuriyet Üniversitesi, 2023) Yulak, Fatih; Filiz, Ahmet Kemal
Kanser, ciddi ekonomik ve sosyal sorunlara neden olan bir halk sağlığı sorunudur. Birçok kanser türü arasında, kolon kanseri en sık teşhis edilen üçüncü kanserdir ve kansere bağlı ölümlerin ikinci önde gelen nedeni olmaya devam etmektedir. Kolon kanseri tedavisinde birçok kemoterapötik ajan kullanılmasına rağmen ideal kemoterapötik ajan arayışı devam etmektedir. Bu bağlamda pek çok yol ve mekanizma öne çıkmaktadır. Bu yollardan birisi de PI3K aracılı yoldur. PI3K aracılı yolak, bir dizi hormona ve büyüme faktörüne yanıt veren hücre içi sinyal yolağıdır. Bu yolağın aktivasyonu, hücre büyümesi, hücre proliferasyonu, hayatta kalma ve artan hücre göçü, ayrıca düzensiz apoptoz ve onkogenez gibi hücresel süreçleri modüle etmektedir. PI3K/AKT/mTOR yolağı deregülasyonu birçok insan kanserinde tümöral hücre proliferasyonu, büyüme ve apoptozisinde önemli rol oynamaktadır. Bu bilgiler ışığında çalışmamızda bir PI3K/AKT/mTOR yolağı inhibitörü olan ETP 45658'in kolon kanseri üzerine antiproliferatif etkinliğinin araştırılması hedeflenmiştir. Çalışmamızda 1, 10, 25, 50, 100 ?M dozlarda ETP 45658, HT-29 kolon kanseri hücrelerine uygulanarak XTT hücre canlılığı testi ile sitotoksik etkisi değerlendirilmiştir. Elde edilen verilerden ETP 45658'in IC50 değeri hesaplanmıştır. Hücrelere belirlenen IC50 doz verilmiştir ve flow sitometri ile apoptoz, hücre döngüsü, mitokondri zar potansiyeli, kaspaze 3/7 çalışmaları yapılmıştır. Belirlenen IC50 değeri hücreye uygulandıktan sonra elisa ile bax, bcl, kaspaz 3, parp ve 8-oxo-dG miktarları ve TAS, TOS değerleri ölçülmüştür. Aynı doz uygulandıktan sonra hücrelere DAPİ boyası verilerek ETP 45658'in sitotoksik etkisinin altında yatan moleküler mekanizmaların aydınlatılması amaçlanmıştır. Elde ettiğimiz XTT sonuçlarına göre ETP 45658 doz bağımlı bir şekilde HT-29 kolon kanseri hücreleri üzerine istatistiksel olarak anlamlı bir antiproliferatif etki göstermiştir. Hesaplanan IC50 dozu ile yapılan ileri çalışmalarda ETP 45658 hücre döngüsünü G0/G1 fazında durdurmuş, apoptotik proteinleri artırıp anti apoptotik proteinleri azaltmış, TAS seviyesini azaltıp TOS seviyesini artırmış ve mitokondri zar potansiyelini depolarize hale getirerek HT-29 kolon kanseri hücrelerinde apoptozisi indüklemiştir. Sonuç olarak ETP 45658'in antiproliferatif etkisi, hücre döngüsünü durdurması ve apoptotik proteinleri artırması ile HT-29 kolon kanseri hücreleri üzerinde apoptozisi uyararak antikanser etkinliği olduğu gösterilmiştir. ETP 45658'in bu etkisi dikkate alındığında kolon kanserli hastalarda PI3K/AKT/mTOR yolağının hedeflenmesi yeni bir tedavi seçeneği olabileceği düşünülmektedir. Ancak bu konuyla ilgili daha fazla hem in vitro hem in vivo çalışmaya ve klinik faz çalışmalarına ihtiyaç vardır.
Evaluation of the Antitumor Activity of Omipalisib, a PI3K/AKT/MTOR Pathway Inhibitor, on Burkitt Lymphoma Cell Line
(2023) Keskin, Zekeriya; Yulak, Fatih; Terzi, Hatice; İnanır, Merve
There are many challenges in the treatment of Burkitt lymphoma, especially in immunocompromised individuals, elderly patients, and patients with relapsed or refractory disease. Therefore, there is a need for new and less toxic therapeutic agents. The aim of this study was to determine the antitumoral activity of omipalisib, a PI3K/AKT/mTOR pathway inhibitor, in the Burkitt lymphoma. Raji cell line was used in the study. Omipalisib was administered to the cell line and then the cytotoxic effect of omipalisib on Raji cells was evaluated by the XTT test. The IC50 value was calculated according to the results of the XTT test. Apoptosis and cell cycle experiments were studied with the calculated IC50 value. The flow cytometric method was used to determine the effect of omipalisib on apoptosis and cell death. The results of the study showed a statistically significant cytotoxic effect of increasing concentrations of omipalisib on Raji cells. The apoptosis experiment performed revealed that omipalisib strongly induced apoptosis. The cell cycle experiment showed that omipalisib stimulated the cell cycle arrest at the G0/G1 phase. It was concluded that omipalisib exhibited antitumoral activity on Burkitt lymphoma cells with its cytotoxic effect and induced apoptosis and cell cycle arrest. Considering this effect, targeting the PI3K/AKT/mTOR pathway with omipalisib can be a new treatment option.
FGF-18 alleviates memory impairments and neuropathological changes in a rat model of Alzheimer’s disease
(Temmuz 2023) Çiltaş, Arzuhan Yeşildağ; Karabulut Sebahattin; Şahin, Bilal; Filiz, Ahmet Kemal; Yulak, Fatih; Özkaraca, Mustafa; Karatas, Özhan; Çetin, Ali
Alzheimer’s disease (AD) is a multifactorial pathology marked by amyloid beta (Aβ) accumulation, tau hyper phosphorylation, and progressive cognitive decline. Previous studies show that fibroblast growth factor 18 (FGF18) exerts a neuroprotective effect in experimental models of neurodegeneration; however, how it affects AD pathology remains unknown. This study aimed to ascertain the impact of FGF18 on the behavioral and neuropathological changes in the rat model of sporadic AD induced by intracerebroventricular (ICV) injection of streptozotocin (STZ). The rats were treated with FGF18 (0.94 and 1.88 pmol, ICV) on the 15th day after STZ injection. Their cognitive function was assessed in the Morris water maze and passive avoidance tests for 5 days from the 16th to the 21st days. Aβ levels and histological signs of neurotoxicity were detected using the enzyme linked immunosorbent assay (ELISA) assay and histopathological analysis of the brain, respectively. FGF18 mildly ameliorated the STZ-induced cognitive impairment; the Aβ accumulation was reduced; and the neuronal damage including pyknosis and apoptosis was alleviated in the rat brain. This study highlights the promising therapeutic potential for FGF18 in managing AD.
GSK461364A suppresses proliferation of gastric cancer cells and induces apoptosis
(Pergamon-Elsevier Science Ltd, 2023) Ataseven, Dilara; Tastemur, Seyma; Yulak, Fatih; Karabulut, Sebahattin; Ergul, Mustafa
Polo-like kinase 1 (PLK1) is crucial in regulating cell division and has been shown to have an oncogenic function in several cancers. Since PLK1 overexpression is closely related to tumorigenesis and has been correlated with poor clinical outcomes, specific inhibition of PLK1 in cancer cells is a promising approach for developing new anticancer drugs. In this context, the aim of the present study was to evaluated the potential cytotoxic effects of GSK461364A, a competitive inhibitor for PLK1, in gastric cancer cell line SNU-1 cells and explored its cytotoxic mechanism. The cells were exposed to GSK461364A at different concentrations ranging from 1 to 40 mu M for 24 h, and it showed considerable cytotoxicity with an IC50 value of 4.34 mu M. The treatment of SNU-1 cells with GSK461364A results in cell cycle arrest at the G2/M phase, decreased mitochondrial membrane potential, and increased apoptosis as indicated by Annexin V binding assay. In addition, GSK461364A treatment significantly increased the total oxidant (TOS) level, a signal of oxidative stress, and increased cleaved PARP and 8-oxo-dG levels as an indicator of DNA damage. ELISA experiments evaluating Bax, BCL-2, and cleaved caspase 3 also confirmed the apoptotic effect of GSK461364A. Current findings suggest that GSK461364A may be a chemotherapeutic agent in patients with gastric cancer. Nevertheless, more research is needed to evaluate GSK461364A as a cancer treatment drug.
HER-2 SMASH
(Springer, 2025) Alandag, Celal; Ozturk, Ayseguel; Yulak, Fatih; Inan, Zeynep Deniz Sahin; Karaca, Mustafa; Lacin, Burak Batuhan; Altun, Ahmet
PurposeHuman epidermal growth factor-2 (HER-2) targeted drugs are used in only HER-2 overexpressed cancers. However, only a small portion of these cancer types are HER-2 overexpressed. In this study, we aimed to upregulate HER-2 receptors in MCF-7 breast cancer and HT-29 colon cancer cell cultures, which these cells are not HER-2 upregulated in natural status.MethodsWe used a 10-day non-cytotoxic lapatinib dose to upregulate HER-2 receptors. HER-2 levels of these cell lines were tested with ELISA and immunofluorescence tests before and after 10 days of lapatinib administration. After upregulation of HER-2, we administered trastuzumab, and T-DM1 to these cell lines to observe whether there is an increase in anticancer activity. We used a cell viability test to show the cytotoxicity of trastuzumab and T-DM1. Also, we used ELISA and immunofluorescence for HER-2 pathway proteins to understand the mechanism of increased anti-cancer activity.ResultsWe showed that administration of lapatinib for 10 days leads to overexpression of HER-2 receptors on both MCF-7 and HT-29 cells. A significant increase in the cytotoxicity of trastuzumab or T-DM1 was observed after 10 days of lapatinib administration.ConclusionWe named this method the smash method, which is the volleyball term. In volleyball, the ball is raised while low and quickly hits the ground again, just like we do with the HER-2 receptor. The smash method can switch HER-2 negative or HER-2 low tumors into HER-2 overexpressed, iatrogenically. Thus, we can use her2-targeted therapies in all cancer patients instead of a small portion.
HER-2 SMASH (vol 95, 10, 2025)
(Springer, 2025) Alandag, Celal; Ozturk, Aysegul; Yulak, Fatih; Sahin Inan, Zeynep Deniz; Ozkaraca, Mustafa; Lacin, Burak Batuhan; Altun, Ahmet
[No abstract available]
Investigation of The Antiproliferative Effect of Colchicine on SNU-1 Gastric Cancer Cells
(2023) Yulak, Fatih
In this study, colchicine's cytotoxic effects on SNU-1 cells were examined, and a probable mechanism behind its cytotoxicity was revealed. According to the results of the study, colchicine displayed considerable cytotoxicity with an IC50 value of 14.81ng/ml when it was administered to the cells for 24 hours at different doses ranging from 5 to 100ng/ml. Furthermore, according to mechanistic studies, usege of colchicine significantly increased both early and late apoptotic cells in flow cytometry experiments. The late apoptotic cell population percentage in the control group (5.14 ± 1.27%) dramatically increased to 22.83 ± 1.38% in 14.81ng/ml colchicine treated cells. The early apoptotic cell population percentage in the control group (2.00 ± 1.12%) increased to 6.57 ± 2.35% in 14.81ng/ml colchicine treated cells. ELISA method was used to evaluate how colchicine affects the expression of pro- and anti-apoptotic proteins in SNU-1 cells. Colchicine treatment increased pro-apoptotic Bax and cleaved caspase 3 activities, while anti-apoptotic BCL-2 levels decreased. It is concluded that colchicine increases apoptosis in SNU-1 cells, which leads to an overall increase in cell death. Colchicine's promise as an anticancer drug to treat stomach cancer, however, needs additional research to be determined.
Investigation of the Effect of Indatraline on Oxidative Damage Induced by Hydrogen Peroxide in C6 Glioma Cell Line
(2023) Yulak, Fatih; Üngür, Bünyamin
Oxidative stress is defined as an imbalance between the generation of reactive oxygen species (ROS) and their scavenging. Indatralin, which has serotonin reuptake inhibitory activity, has not yet been studied for its ability to prevent oxidative damage. Our research's objective was to find out how indatraline defends against oxidative damage. C6 cells were used in the study and four different cell groups were created. The control group received no therapy at all. For 24 hours, cells in the H2O2 group were exposed to 0.5 mM H2O2. The indatraline group received indatraline treatments for 24 hours at various doses (0.5, 1, 2.5, 5 and 10 ?M). For one hour, indatraline was administered to the indatraline + H2O2 group at various concentrations (0.5, 1, 2.5, 5 and 10 ?M) before the group was subjected to 0.5 mM H2O2 for 24 hours. Following the occurrence of oxidative damage, total antioxidant status (TAS) and total oxidant status (TOS) levels were determined. Cell viability was also evaluated using the XTT assay. As a result, after hydrogen peroxide-induced oxidative damage, indatraline at doses of 10, 5, and 2.5 ?M showed a protective effect by significantly enhanced cell survival in C6 cells(p < 0.001). Additionally, indatraline boosted the lowered TAS level while decreasing the elevated TOS levels following hydrogen peroxide-induced oxidative damage (p<0.001).
Investigation of the potential antitumor activity of PLK1 inhibitor SBE13 in colon cancer cell line HT29
(Sivas Cumhuriyet University, 2022) Gömeç, Muhammed; Yulak, Fatih; Ergül, Mustafa
Background: High levels of Polo-like kinase 1 (PLK1), which are abnormally expressed in many tumor types, are known to contribute to tumorigenesis and poor prognosis. Therefore, specific targeting of PLK1 is an important strategy for cancer therapy. This study, it was aimed to investigate the cytotoxic effect of SBE13, one of the PLK1 inhibitors, against HT29 colon adenocarcinoma cells and its apoptotic potential.Methods: The cytotoxic effect of SBE13 on HT29 was determined by XTT colorimetric assay. Flow cytometry was also used to determine apoptosis.Results: SBE13 showed a dose-dependent cytotoxic effect in HT29 cells and its IC50 value was calculated as 11.79 µM for 48 h. Moreover, the Annexin V binding assay revealed that SBE13 treatment significantly increased apoptosis in HT29 cells.Conclusion: Generally, SBE13 exerts a cytotoxic effect promoted by apoptosis in colon cancer cells HT29. Although the anticancer efficacy of SBE13 in colon cancer is promising, this potential effect should be reinforced by further studies.
Levetiracetam Protects Against Glutamate-Induced Excitotoxicity in SH-SY5Y Cell Line
(Uğur ÇAKILCIOĞLU, 2022) Çiltaş, Arzuhan Çetindağ; Gündoğdu, Sema; Yulak, Fatih
The latest research has shown that the new generation of antiepileptic drugs has neuroprotective on nervous system. On the other hand, the effect of levetiracetam, a new generation antiepileptic drug, on GIC in SH-SY5Y cells remains uncertain. This research aims to investigate the effect of levetiracetam on GIC and oxidant and antioxidant levels in SH-SY5Y cells. It is utilized SH-SY5Y cell line at this research. Four groups were formed to assess the impact of levetiracetam on SH-SY5Y cell death following GIC. While no treatment was administered to the control group, 10 mM glutamate was administered to the glutamate group for 24 hours (10, 25, 50 and 100 μg/ml). LEV at different concentrations was given to the levetiracetam for 24 hours. The levetiracetam + glutamate was pretreated with levetiracetam at several concentrations for 1 hour (10, 25, 50, and 100 μg/ml), which was followed by a 24-hour exposure to 10 mM glutamate. TAS and TOS levels in cells and cell viability were examined. Following the GIC, a 25 μg/ml-Levetiracetam improved cell viability in neuroblastoma cells dramatically (p < 0.05). LEV (25 ug/ml) + glutamate while enhanced TAS levels in neuroblastoma cells in comparison to the glutamate (p < 0.05), significantly reduced TOS levels (p < 0.05 Levetiracetam improves cell survival by reducing cell death following GIC in neuroblastoma cells. In the acute process, levetiracetam exerts a protective effect.
Lycopene induces antiproliferative effects through apoptosis, autophagy, and oxidative DNA damage in the HeLa cells
(Taylor & Francis Ltd, 2024) Parlak, Mesut; Joha, Ziad; Yulak, Fatih; Mendil, Ali Sefa; Tastemur, Yasar
Background: This study explores the role of apoptosis, autophagy, and oxidative DNA damage in influencing the cytotoxic impact of lycopene on HeLa cells. Material and methods: Cell viability following exposure to varying lycopene concentrations was determined using an XTT assay. ELISA measured key cell death proteins (Bax, BCL-2, etc.), while immunofluorescence staining visualized LC3 beta (autophagy) and 8-oxo-dG (DNA damage). Results: Lycopene significantly killed HeLa cells in a dose-dependent way (IC50 = 10 mu M). Subsequent examinations conducted with the IC50 dose of lycopene demonstrated a notable elevation in the expression levels of apoptotic proteins, such as cleaved caspase 3, cleaved PARP, and Bax (p < 0.001). Additionally, treatment with this substance led to an increase in the levels of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicative of oxidative DNA damage. Furthermore, a significant rise (p < 0.05) in LC3 beta protein levels, a well-established indicator of autophagy activation, was noted. Conclusion: This study suggests lycopene's potential to fight cervical cancer by triggering programmed cell death (apoptosis) and cellular self-digestion (autophagy). These findings highlight lycopene as a promising candidate for future cervical cancer treatments.
Mechanism of anti-cancer effect of ?-glucan on SH-SY5Y cell line
(Bangladesh Pharmacological Soc, 2021) Filiz, Ahmet Kemal; Joha, Ziad; Yulak, Fatih
Anti-cancer property of fungi derived 13-glucan (Lentinula edodes) on several cancer cell lines have been reported. In this work, the SH-SY5Y cell lines were treated with various concentrations of 13-glucan (62.5, 125, 250 and 500 pg/mL) and the viability of the cells was tested using the XTT assay after 24 hours. Cleaved PARP, BCL-2, 8-hydroxy-desoxyguanosine (8-oxo-dG), cleaved caspase 3, Bax, total oxidant, and total antioxidant levels in the cells were measured by commercial kits. 13-Glucan significantly decreased the cell viability in SH-SY5Y cells. ELISA tests demonstrated that 13-glucan therapy dramatically increased 8-oxo-dG, cleaved caspase 3, Bax, cleaved PARP, total oxidant. However, 13-glucan treatment did not change the BCL-2 protein level. Altogether, 13-glucan caused significant cytotoxicity in SH-SY5Y cells by inducing oxidative stress, increasing DNA damage, and ultimately increasing apoptosis.
Mechanism of anticancer effect of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor on HT-29 Cells
(Humana Press Inc, 2023) Yulak, Fatih; Filiz, Ahmet Kemal; Joha, Ziad; Ergul, Mustafa
The PI3K pathway plays a crucial role in tumor cell proliferation across various cancers, including colon cancer, making it a promising treatment target. This study aims to investigate the antiproliferative activity of ETP-45658, a PI3K/AKT/mTOR pathway inhibitor, on colon cancer and elucidate the underlying mechanisms. HT-29 colon cancer cells were treated with varying doses of ETP 45658 and its cytotoxic effect assessed using the XTT cell viability assay.ELISA was also used to measure TAS, TOS, Bax, BCL-2, cleaved caspase 3, cleaved PARP, and 8-oxo-dG levels. Flow cytometry was performed to investigate apoptosis, cell cycle, caspase 3/7 activity, and mitochondrial membrane potential. Additionally, following the administration of DAPI (4,6-diamidino-2-phenylindole) dye, the cells were visualized using an immunofluorescence microscope. It was observed that ETP-45658 exerted a dose-dependent and statistically significant antiproliferative effect on HT-29 colon cancer cells. Further investigations using the IC50 dose showed that ETP-45658 decreased TAS levels and increased TOS levels and revealed that it upregulated apoptotic proteins while downregulating anti-apoptotic proteins. Our findings also showed that it increased Annexin V binding, arrested the cell cycle at G0/G1 phase, induced caspase 3/7 activity, impaired mitochondrial membrane potential, and ultimately triggered apoptosis in HT-29 cells. ETP-45658 shows promise against colon cancer by inducing cell death, and oxidative stress, and arresting the cell cycle. Targeting the PI3K/AKT/mTOR pathway with ETP-45658 offers exciting potential for colon cancer treatment.
Mechanism of anticancer effect of gambogic acid on gastric signet ring cell carcinoma
(Humana Press Inc, 2023) Joha, Ziad; Ozturk, Aysegul; Yulak, Fatih; Karatas, Ozhan; Ataseven, Hilmi
Gambogic acid has demonstrated inhibitory effects on the growth of various cancer cell types, such as breast cancer, pancreatic cancer, prostate cancer, lung cancer, and osteosarcoma. This study aims to investigate the antiproliferative activity of Gambogic acid on SNU-16 cells derived from gastric signet ring cell carcinoma and elucidate the underlying mechanisms. The cytotoxic effect of gambogic acid was evaluated in SNU-16 cells by treating them with different concentrations of the compound, and the XTT cell viability assay was employed to assess cell viability. ELISA was used to measure bax, BCL-2, caspase 3, PARP, and 8-oxo-dG levels. Additionally, immunofluorescence staining was applied to assess 8-oxo-dG and LC3 & beta; levels in SNU-16 cells. It was observed that gambogic acid exerted a dose-dependent and statistically significant antiproliferative effect on SNU-16 cells. The IC50 value of gambogic acid in SNU-16 cells was found to be 655.1 nM for 24 h. Subsequent investigations conducted using the IC50 dose revealed a significant upregulation of apoptotic proteins including cleaved caspase 3, Bax, and cleaved PARP (p < 0.001), along with a downregulation of BCL-2 (p < 0.001), an anti-apoptotic protein. Moreover, the administration of this drug led to an upregulation of 8-oxo-dG (p < 0.001), a widely acknowledged biomarker indicating oxidative damage in DNA, as well as an increase in LC3 & beta; levels (p < 0.05), a marker associated with autophagy. The antiproliferative effect of gambogic acid against gastric signet ring cell carcinoma is attributed to its ability to induce apoptosis and autophagy. This discovery highlights the promising potential of gambogic acid as a treatment option for gastric signet ring cell carcinoma.
Tannic acid protects neuroblastoma cells against hydrogen peroxide - triggered oxidative stress by suppressing oxidative stress and apoptosis
(Elsevier, 2024) Yulak, Fatih; Ergul, Mustafa
Recent investigations indicate that tannic acid is associated with a decrease in oxidative damage. Growing evidence supports the protective effects of tannic acid on the central nervous system (CNS). However, uncertainties persist regarding its influence on hydrogen peroxide (H2O2)-triggered oxidative impairment in nerve cells and its interaction with apoptosis. Hence, the objective of this work was to examine the neuroprotective impact of tannic acid on SH-SY5Y cell impairment following H2O2-induced oxidative stress, particularly concerning apoptotic pathways. The control group received no treatment, while the H2O2 group underwent treatment with 0.5 mM H2O2 for a duration of 24 h. The tannic acid group received treatment with different concentrations of tannic acid for a duration of 24 h. Meanwhile, the tannic acid + H2O2 group underwent pre-treatment with tannic acid for one hour and was subsequently subjected to 0.5 mM H2O2 for one day. Within the tannic acid + H2O2 group, the cell viability in SH-SY5Y cells was notably enhanced by tannic acid at concentrations of 2.5, 5, and 10 mu M. It also resulted in a considerable rise in TAS (Total Antioxidant Status) levels and a concurrent decline in TOS (Total Oxidant Status) levels, serving as indicators of reduced oxidative stress. Additionally, tannic acid treatment resulted in decreased levels of apoptotic markers (Bax, cleaved PARP, and cleaved caspase 3) and oxidative DNA damage marker (8-oxo-dG), while increasing the anti-apoptotic marker Bcl-2. The findings from flow cytometry also revealed a significant reduction in the apoptosis rate following pretreatment with tannic acid. In summary, tannic acid demonstrates protective effects on SH-SY5Y cells in the face of H2O2-triggered oxidative damage by suppressing both oxidative stress and apoptosis. Nevertheless, additional research is warranted to assess the neuroprotective potential of tannic acid.
Unveiling the Protective Potential of Sugammadex against PTZ-Induced Epileptic Seizures in Mice: A Comprehensive Study on Oxidative Stress, Apoptosis, and Autophagy
(Maik Nauka/Interperiodica/Springer, 2024) Karademir, Mustafa; Ozturk, Aysegul; Yulak, Fatih; Ozkaraca, Mustafa; Taskiran, Ahmet Sevki
Sugammadex (SUG) is a modified gamma-cyclodextrin molecule used in patients under general anesthesia to reverse the effects of neuromuscular blocking agents. Besides, recent studies have shown that SUG positively affects the nervous system. However, its effect on seizures is still unclear. The current study aimed to examine the effects of SUG on pentylenetetrazole (PTZ)-induced epileptic seizures in mice. The mice were randomly divided into four groups. Group 1 was controlled, group 2 was administered saline (1 mL/kg serum physiologic), and Groups 3 and 4 were administered Sugammadex (150 and 300 mg/kg). Pentylenetetrazole (60 mg/kg) was given to induce seizures 30 min after saline or drug administration except for the control group. Total oxidant status (TOS) and total antioxidant status (TAS) levels in the hippocampus and cortex were measured using a commercial kit. 8-hydroxydeoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), 3,3 dityrosine, caspase-3, apoptosis-inducing factor (AIF), and light chain 3 (LC3B) levels in the hippocampal CA1 region and cortex after seizures were evaluated immunohistochemical staining. SUG reduced seizure stages and increased epileptic seizure onset times. Moreover, it decreased TOS levels and increased TAS levels in the hippocampus and cortex. Besides, after seizures, it reduced 4-HNE, 3,3 dityrosandine, caspase-3, and LC3B immunohistochemical scores in the hippocampal CA1 region and cortex. SUG has protective effects on pentylenetetrazole-induced seizures in mice, alleviating seizures, oxidative stress, apoptosis, and autophagy. The anticonvulsant mechanism of SUG may be related to the inhibition of the oxidative stress pathway.

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