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Öğe Assessing effects of caffeic acid on cytotoxicity, apoptosis, invasion, GST enzyme activity, oxidant, antioxidant status and micro-RNA expressions in HCT116 colorectal cancer cells(Elsevier, 2023) Secme, Mucahit; Mutlu, Dogukan; Elmas, Levent; Arslan, SevkiIn developed western countries, colorectal cancer is one of the most prevalent cancer types. Natural bioactive compounds attract attention due to their antioxidant, anti-inflammatory, anticancer and therapeutic activities. Caffeic acid (3,4-dihydroxycinnamic) is one of the one of the most common phenolic acids found in many foods and plants such as coffee, honey, blueberries, herbs, potatoes, apples. The aim of the study is investigating cytotoxic, apoptotic, anti-invasive, oxidant, antioxidant, GST inhibitory activities of caffeic acid in colon cancer cells. Another aim of this study is to demonstrate a mechanistic approach by investigating the expression changes of mRNA and micro RNAs that play a role in these cellular mechanisms. In this context, MTT, Annexin-V, Matrigel invasion, TAS-TOS, GST enzyme activity assay and Real-Time PCR experiments were performed under in vitro conditions. According to results, caffeic acid have exhibits antiproliferative, apoptotic and anti-invasive activity in HCT116 cells. It caused changes expression of apoptosis, cell cycle and invasion-related genes and microRNAs. Caffeic acid also reduced oxidative stress and GST enzyme activity. Taken together, all these results reveal that caffeic acid may be a therapeutic agent in HCT116 colorectal cancer cells. This study will shed light on future comprehensive studies. (c) 2023 SAAB. Published by Elsevier B.V. All rights reserved.Öğe Erianin, a promising agent in the treatment of glioblastoma multiforme triggers apoptosis in U373 and A172 glioblastoma cells(Inst Bioloska Istrazivanja Sinisa Stankovic, 2022) Kocoglu, Sema Serter; Secme, Mucahit; Elmas, LeventGlioblastoma is an aggressive, common and deadly primary intracranial brain tumor in adults. The antitumor activity of erianin, a dibenzyl compound found in Dendrobium chrysotoxum Lindl. extract, has not been previously demonstrated in glioblastoma. We investigated the anticancer activity and underlying mechanisms of erianin in human U373 and A172 glioma cells. The effects of erianin on cell viability, apoptosis, migration and invasion were estimated by the XTT test, the reverse transcription-polymerase chain reaction (RT-PCR), annexin V staining assay protocol for apoptosis, wound healing assay, and Matrigel (R) invasion chamber, respectively. The effective amounts of erianin in U373 and A172 cells were 16 and 64 mu M at 48 h, respectively. Erianin also significantly induced apoptosis by inhibiting B-cell lymphoma 2 (Bcl-2), caspase-8, caspase-9 and tumor necrosis factor receptor type 1-associated DEATH domain protein (TRADD), and activation of caspase-3 and BH3 interacting domain death agonist (BID) gene expression. In addition, erianin significantly increased the number of apoptotic cells in U373 and A172 cells and significantly decreased invasion and migration in U373 and A172 cells. Taken together, our results suggest that erianin may be a new therapeutic anticancer drug component with a potent apoptotic effect and a potential for treating glioblastoma.Öğe Erianinin HT29 kolorektal kanser hücrelerinin proliferasyonu ve koloni oluşumu üzerine etkilerinin araştırılması(2021) Seçme, Mücahit; Elmas, Levent; Koçoğlu, Sema SerterKolorektal kanser, dünyada kanser ilişkili ölümlerin en yaygın dördüncü sebebidir. Erianin antioksidan ve anti-tümör etkilere sahip Dendrobium ekstraktından elde edilen yeni bir dibenzil bileşiğidir. Bu çalışmada, erianinin HT29 kolorektal kanser hücreleri üzerine olan terapötik etkileri araştırılmıştır. Erianinin HT29 hücre canlılığı üzerine etkileri XTT test ile koloni oluşumu üzerine etkileri ise koloni formasyonu ile değerlendirilmiştir. Erianinin HT29 hücrelerinde IC50 değeri 48. saatte 59.05 ?M olarak belirlenmiştir. HT29 hücre dizisinde erianin uygulanan grupta koloni sayısı 67±33 iken kontrol grubunda 350±89 olarak hesaplanmıştır. Erianin, HT29 kolorektal kanser hücrelerinde koloni oluşumunu ise anlamlı derecede azaltmıştır. Yapılan çalışmaların sonuçları, erianinin kolorektal kanser tedavisinde doğal elde edilen bir bileşik olarak güvenli, kolay ulaşılabilir ve umut veren terapötik bir ilaç olabileceğini destekler niteliktedir. Gelecekte erianinin kolorektal kanser hücreleri üzerindeki etki mekanizmasını aydınlatacak daha kapsamlı ve çok merkezli desteklenecek ileri düzeyde klinik çalışmalara ihtiyaç vardır.Öğe Glycoside oleandrin downregulates toll-like receptor pathway genes and associated miRNAs in human melanoma cells(Elsevier, 2022) Güneş, Canan Eroğlu; Çelik, Fatma Seçer; Seçme, Mücahit; Elmas, Levent; Dodurga, Yavuz; Kurar, ErcanMelanoma accounts for the majority of skin cancer-related deaths. Nerium oleander is a plant known to be toxic and consumed due to the cardiac glycosides it contains. Oleandrin is a cardiac glycoside obtained from of N. oleander. Beside capable of inhibiting proliferation and metastasis of cancer cells, cardiac glycoside derivative compounds cause cardiovascular side effects. Because of cardiovascular toxicity of clinically used cardiac gly-cosides, it is necessary to investigate cardiac glycoside derivative compounds capable of inhibiting proliferation and metastasis of cancer cells.It is known that oleandrin has anticarcinogenic effects in other cancers. Previous studies have shown that toll -like receptors (TLRs) and their related microRNAs (miRNAs) are associated with cancer. Therefore, aim was to investigate the effect of oleandrin on genes and miRNAs associated with TLRs in A375 melanoma cells in this study. The effects of oleandrin on cell viability, cytokines, apoptosis were evaluated using XTT, ELISA and TUNEL analyses, respectively. The effect of oleandrin on expression of TLR genes and 5 associated miRNAs in A375 cells has been determined by qRT-PCR. In addition, the levels of MyD88, TLR2 and TLR4 proteins were analyzed by western blot method.ELISA indicated that oleandrin treatment (47 nM at 48 h) reduced the level of proinflammatory cytokine IFNG. TUNEL analysis showed that apoptosis rate was significantly increased in the oleandrin dose group. According to qRT-PCR results, there was a significant decrease in IRAK1, IRAK4, MyD88, TLR2-TLR7 and TRAF3 expressions in the oleandrin treated group compared to the control (untreated cell). Also, a significant decrease in TLR4 protein expression has been observed. In addition, oleandrin significantly downregulated the levels of hsa-miRNA-146a-5p and hsa-miRNA-21-5p.In conclusion, it has been observed that oleandrin has an effect on TLR pathway-related genes and miRNAs in melanoma cells. We show that TLRs pathways and hsa-miR-146a-5p and hsa-miR-21-5p can participate in the oleandrin molecular mechanism of action.Öğe Monensin, an Antibiotic Isolated from Streptomyces Cinnamonensis, Regulates Human Neuroblastoma Cell Proliferation via the PI3K/AKT Signaling Pathway and Acts Synergistically with Rapamycin(Mdpi, 2023) Kocoglu, Sema Serter; Secme, Muecahit; Oy, Ceren; Korkusuz, Gozde; Elmas, LeventNeuroblastoma is the most common extracranial childhood tumor and accounts for approximately 15% of pediatric cancer-related deaths. Further studies are needed to identify potential therapeutic targets for neuroblastoma. Monensin is an ionophore antibiotic obtained from Streptomyces cinnamonensis with known antibacterial and antiparasitic effects. No study has reported the effects of monensin on SH-SY5Y neuroblastoma cells by targeting the PI3K/AKT signaling pathway. The aim of this study was to investigate the antiproliferative effects of monensin alone and in combination with rapamycin in human SH-SY5Y neuroblastoma cells mediated by the PI3K/AKT signaling pathway. The effects of single and combination applications of monensin and rapamycin on SH-SY5Y cell proliferation were investigated by XTT, and their effects on the PI3K/AKT signaling pathway by RT-PCR, immunohistochemistry, immunofluorescence, and Western blotting. The combined effects of monensin and rapamycin on SH-SY5Y proliferation were most potent at 72 h (combination index < 1). The combination of monensin and rapamycin caused a significant decrease in the expression of P21RAS, AKT, and MAPK1 genes. Single and combined administrations of monensin and rapamycin caused a significant decrease in PI3K/AKT expression. Our results showed for the first time that monensin exerts an antiproliferative effect by targeting the PI3K/AKT signaling pathway in neuroblastoma cells. It is suggested that monensin and its combination with rapamycin may be an effective therapeutic candidate for treating neuroblastoma.Öğe The role of ERK-1 and ERK-2 gene polymorphisms in PCOS pathogenesis(Bmc, 2022) Guney, Gurhan; Taskin, Mine Islimye; Sener, Nazli; Tolu, Ezgi; Dodurga, Yavuz; Elmas, Levent; Cetin, OrkunBackground Ovulation is regulated by extracellular signal-regulated kinase-1 (ERK-1) and ERK-2 signaling mechanisms, and ERK-1/2 kinases modulates the function of most of the LH-regulated genes. Defective ERK kinase signaling that is secondary to a genetic problem contributes to both ovulatory dysfunction and metabolic problems in polycystic ovary syndrome (PCOS). We planned to investigate ERK-1 and ERK-2 gene polymorphisms in PCOS for the first time in the Turkish population. Methods One hundred two PCOS patients and 102 healthy controls were recruited for this patient control study. HOMA-IR, Ferriman-Gallwey score (FGS), waist-to-hip ratio (WHR), and body mass index (BMI) were assessed. Lipid profile levels, CRP, and total testosterone were determined. ERK-2 rs2276008 (G > C) and ERK-1 rs11865228 (G > A) SNPs were analyzed with a real-time PCR system. Results ERK-1 and ERK-2 genotypes were found to differ between the PCOS and control groups. In patients with PCOS, ERK-1 GA and ERK-2 GC genotypes were different in terms of BMI, FGS, HOMA-IR, CRP, total testosterone, and total cholesterol levels. Conclusions ERK-1 and ERK-2 genes are involved in PCOS pathogenesis. BMI, FGS, HOMA-IR, and CRP levels are related to the heterozygote polymorphic types of ERK-1 and ERK-2 genes.
