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    Autophagic mechanisms in longevity intervention: role of natural active compounds
    (Cambridge Univ Press, 2023) Akca, Kevser Taban; Ayan, Ilknur Cinar; Cetinkaya, Sumeyra; Salihoglu, Ece Miser; Suntar, Ipek
    The term 'autophagy' literally translates to 'self-eating' and alterations to autophagy have been identified as one of the several molecular changes that occur with aging in a variety of species. Autophagy and aging, have a complicated and multifaceted relationship that has recently come to light thanks to breakthroughs in our understanding of the various substrates of autophagy on tissue homoeostasis. Several studies have been conducted to reveal the relationship between autophagy and age-related diseases. The present review looks at a few new aspects of autophagy and speculates on how they might be connected to both aging and the onset and progression of disease. Additionally, we go over the most recent preclinical data supporting the use of autophagy modulators as age-related illnesses including cancer, cardiovascular and neurodegenerative diseases, and metabolic dysfunction. It is crucial to discover important targets in the autophagy pathway in order to create innovative therapies that effectively target autophagy. Natural products have pharmacological properties that can be therapeutically advantageous for the treatment of several diseases and they also serve as valuable sources of inspiration for the development of possible new small-molecule drugs. Indeed, recent scientific studies have shown that several natural products including alkaloids, terpenoids, steroids, and phenolics, have the ability to alter a number of important autophagic signalling pathways and exert therapeutic effects, thus, a wide range of potential targets in various stages of autophagy have been discovered. In this review, we summarised the naturally occurring active compounds that may control the autophagic signalling pathways.
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    Evaluation of Apoptosis Pathway of Geraniol on Ishikawa Cells
    (Routledge Journals, Taylor & Francis Ltd, 2021) Kuzu, Betul; Cuce, Gokhan; Ayan, Ilknur Cinar; Gultekin, Burcu; Canbaz, Halime Tuba; Dursun, Hatice Gul; Sahin, Zafer
    Endometrial cancer is the most common type of cancer in the female reproductive system. Geraniol is acyclic monoterpene alcohol derived from essential oils of aromatic plants. This study aimed to investigate the apoptosis pathway of geraniol on Ishikawa cells. The cytotoxic effects of Geraniol on Ishikawa cells were determined by an MTT test. Ishikawa cells were seeded on cover slips, the IC50 dose was applied, and the cells were incubated with antibodies against Bax, Bcl-2, and TUNEL Assay. mRNA expression analysis of apoptosis-related genes was determined by RT-qPCR with an IC50 dose of Geraniol. The IC50 dose of Geraniol decreased Bcl-2 staining significantly, but it significantly increased Bax staining and TUNEL positive cells. A significant increase in the Bax, caspase3, caspase-8, cytochrome C and Fas genes and a significant decrease in the Bcl-2 gene was observed when the IC50 dose group was compared to the cells in the control group based on their mRNA expression levels.Analysis of expression of genes whose products are involved in apoptosis suggests the involvement of the mitochondrial pathway.
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    Inhibitory effect of AK-7 mediates by apoptosis, increases DNA fragmentation and caspase-3 activity in human glioblastoma multiforme cells
    (Bangladesh Pharmacological Soc, 2022) Guclu, Ebru; Ayan, Ilknur Cinar; Vural, Hasibe
    Sirtuins (SIRTs) which are nicotinamide adenine dinucleotide (NAD+) dependent class III histondeacetylases have a controversial role in cancer. In this study, the effect of pharmacological inhibition of AK-7, a SIRT2 inhibitor, was investigated in U87 glioblastoma multiforme cells. The cytotoxic effect of AK-7 was evaluated by XTT analysis. After AK-7 treatment, colony forming capacity of cells was determined and apoptosis was evaluated. The expression levels of apoptosis-related genes were determined by qRT-PCR. According to the results, AK-7 inhibited cell proliferation in a dose-and time-dependent manner. After AK-7 treatment, the colony forming capacity of U87 cells was suppressed. And, AK-7 increased apoptosis rate, DNA fragmentation, and caspase-3 activity. According to qRT-PCR, a significant increase was observed in expression levels of apoptosis-related genes. This study revealed that AK-7 inhibits cell proliferation and induces apoptosis in glioblastoma multiforme cells and SIRT2 inhibition can be evaluated as a therapeutic approach in glioblastoma multiforme.
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    Lysates from the probiotic bacterium Streptococcus thermophilus enhances the survival of T cells and triggers programmed cell death in neuroblastoma cells
    (Humana Press Inc, 2023) Altves, Safaa; Guclu, Ebru; Ayan, Ilknur Cinar; Bilecen, Kivanc; Vural, Hasibe
    Neuroblastoma is the most common brain solid tumor in infancy. Despite the availability of numerous approaches like immunotherapy, surgery, chemotherapy, and radiotherapy, neuroblastoma frequently develops resistance and recurs. Immunotherapy is one of the most promising approaches and PD-L1 antibody blocking is the phenomena used to inhibit PD-1 receptors to increase and improve cytotoxic T cells toward cancer. Numerous studies underlined the critical role of probiotics on immune system development and modulation in addition to possible role in inducing apoptosis in cancer cells. In this study, a Streptococcus thermophilus strain, isolated from a local yogurt, was used as it is considered a potential probiotic due to its tolerance lower pH, bile acid, antibiotic suitability, and blood hemolysis. Our results showed that S. thermophilus lysates played as an immune checkpoint modulator at 25 mu g/ml dose boosting PD-L1 transcripts and protein levels in SH-SY5Y neuroblastoma cell line. Interestingly, co-culture between SH-SY5Y and Jurkat T cells in the presence of blocking PD-L1 antibodies increased Jurkat T-cell viability compering to control without lysate. On the other hand, annexin-V/7-AAD, qPCR and western blot results showed that S. thermophilus lysates at 200 and 400 mu g/ml decreased SH-SY5Y cell viability and increased apoptotic marker genes transcription and caspase-3 and caspase-9 protein expression.
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    Piceatannol induces apoptotic cell death through activation of caspase-dependent pathway and upregulation of ROS-mediated mitochondrial dysfunction in pancreatic cancer cells
    (Springer, 2022) Ayan, Ilknur Cinar; Guclu, Ebru; Vural, Hasibe; Dursun, Hatice Gul
    Background Piceatannol is a naturally occurring plant-derived phenolic compound (stilbenoid), an analogue of resveratrol. It has been shown that, piceatannol has biological activity properties such as antiproliferative, antioxidative, anti-inflammatory and proapoptotic, in various human cancer studies in vitro and in vivo. Objectives and methods In this study, it was aimed to investigate whether piceatannol induces apoptosis through anticancer activity methods (cell viability, colony formation, annexin-V/7-AAD, ROS (Reactive oxygen species), MMP (Mitochondrial membrane potential), wound healing, invasion assay, RT-qPCR (Real-Time Quantitative Polymerase Chain Reaction), western blotting in PANC-1 and MIA PaCa-2 pancreatic cancer (PC) cell lines. Results According to our results, piceatannol decreased cell viability in a dose and time-dependent manner [the half-maximal inhibitory concentration (IC50): 60 mu M in PANC-1 and IC50: 90 mu M in MIA PaCa-2 cell line at 48 h (h)] and caused significant changes in the expression of apoptosis-related genes and protein. Piceatannol induced apoptosis in PANC-1 and MIA PaCa-2 cells, accompanied by increased ROS production, decreased MMP, and increased Caspase-3-9 activity. Piceatannol also inhibited colony-forming abilities, invasion, and migration of PC cells. Conclusion Our results show that piceatannol has an anti-cancerogenic effect on PANC-1 and MIA PaCa-2 cells, and exerts this effect by suppressing proliferation and inducing apoptosis. Therefore, piceatannol could be considered to be a potential chemotherapeutic agent candidate for the treatment and prevention of PC. [GRAPHICS] .
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    Tomentosin induces apoptosis in pancreatic cancer cells through increasing reactive oxygen species and decreasing mitochondrial membrane potential
    (Pergamon-Elsevier Science Ltd, 2022) Gueclue, Ebru; Ayan, Ilknur Cinar; Dursun, Hatice Guel; Vural, Hasibe
    The aim of this study was to determine possible anticancer effect of tomentosin, a natural sesquiterpene lactone, on pancreatic cancer cells. The cytotoxic effect of tomentosin was determined by XTT analysis. Colony formation and apoptosis analyzes were performed, Reactive oxygen species (ROS) level and change in mitochondrial membrane potential (MMP) were evaluated in control and tomentosin-treated cells. The effect of tomentosin on expression levels of apoptosis-related genes was determined by qRT-PCR and Caspase-3 and Caspase-9 proteins were analyzed by western blot. And, the effect of tomentosin on migration and invasion of cells were evaluated. The IC50 dose of tomentosin was found to be 31.11 mu M in PANC-1 cells and 33.93 mu M in MIA PaCa-2 cells for 48 h. And, treatment of tomentosin at IC50 dose suppressed the colony forming capacity of cells. While tomentosin increased apoptosis rate and ROS production, an decrease was observed in MMP. Tomentosin affected expression level of apoptosis-related genes and increased Caspase-3 and Caspase-9 protein levels. After tomentosin treat-ment, cell migration and invasion were suppressed. As a result, this study reveals that tomentosin has anticancer effects on pancreatic cancer cells, and therefore it predicts that tomentosin can be evaluated as an effective agent against pancreatic cancer.