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Öğe Association Between Plasma Asprosin Levels and Gestational Diabetes Mellitus(Dove Medical Press Ltd, 2023) Boz, Ibrahim Bekir; Salt, Semra Ayturk; Salt, Omer; Sayin, Niyazi Cenk; Dibirdik, IlkerPurpose: This study sought to investigate whether asprosin can be used in the diagnosis of GDM or for diagnostic purposes in high-risk pregnancies, along with a review of other parameters that may be associated with serum asprosin levels. Patients and Methods: The study investigated the association between gestational diabetes mellitus (GDM) and asprosin levels. A total of 93 participants; 30 patients with GDM, 33 healthy pregnant women with normal glucose tolerance (NGT), and 30 healthy non-diabetic women (control group) at the Endocrinology and Metabolic Diseases outpatient clinic of a tertiary care university hospital were enrolled in the study. Patients with GDM and NGT were examined in terms of GDM between the 24th and 28th week of pregnancy (2nd trimester). Patient data were collected during routine examinations, and asprosin levels were measured using the ELISA method. All participants underwent testing for measurements of serum hemoglobin, insulin, C-peptide, fasting plasma glucose, and glycated hemoglobin (HbA1c) levels following a fasting period of at least eight hours. Results: Asprosin levels were higher in pregnant women with NGT and with GDM versus controls (Control-NGT asprosin, p = 0.001; Control-GDM asprosin, p = 0.001). Pregnant women with GDM had higher asprosin levels than those with NGT (p = 0.001). In detecting GDM in pregnant women, an asprosin cutoff value of >31.709 ng/mL yielded a sensitivity of 93.3%, specificity of 90.9%, positive predictive value of 90.3%, and negative predictive value of 93.75% (p < 0.001). Conclusion: Serum asprosin levels can potentially be used as a marker in the diagnosis of GDM.Öğe The flavonoid apigenin reduces prostate cancer CD44+ stem cell survival and migration through PI3K/Akt/NF-?B signaling(Pergamon-Elsevier Science Ltd, 2016) Erdogan, Suat; Doganlar, Oguzhan; Doganlar, Zeynep B.; Serttas, Riza; Turkekul, Kader; Dibirdik, Ilker; Bilir, AyhanAims: Cancer stem cells (CSCs) are involved in drug resistance, metastasis and recurrence of cancers. The efficacy of apigenin on cell survival, apoptosis, migration and stemness properties were analyzed in CSCs. Main methods: Prostate CSCs (CD44(+)) were isolated from human prostate cancer (PCa) PC3 cells using a magnetic-activated cell sorting system. PC3 and CSCs were treated with various concentrations of apigenin, docetaxel and their combinations for 48 h. Key findings: Apigenin dose dependently inhibited CSCs and PC3 cell survival, and this was accompanied with a significant increase of p21 and p27. Apigenin induced apoptosis via an extrinsic caspase-dependent pathway by upregulating the mRNA expressions of caspases-8,-3 and TNF-alpha, but failed to regulate the intrinsic pathway as determined by the Bax, cytochrome c (Cyt-c) and APAF-1 in CSCs. In contrary to CSCs, apigenin induced intrinsic apoptosis pathway as evidenced by the induction of Bax, Cyt-c and caspase-3 while caspase-8, TNF-alpha and Bcl-2 levels remained unchanged in PC3 cells. The flavonoid strongly suppressed the migration rate of CSCs compared to untreated cells. Significant downregulation of matrix metallopeptidases-2,-9, Snail and Slug exhibits the ability of apigenin treatment to suppress invasion. The expressions of NF-kappa B p105/p50, PI3K, Akt and the phosphorylation of pAkt were decreased after apigenin treatment. Moreover, apigenin treatment significantly reduced pluripotency marker Oct3/4 protein expression which might be associated with the down-regulation of PI3K/Akt/NF-kappa B signaling. Significance: Our data indicated that, apigenin could be a useful compound to prevent proliferation and migration of cancer cells as well as CSCs. (C) 2016 Elsevier Inc. All rights reserved.Öğe Midkine downregulation increases the efficacy of quercetin on prostate cancer stem cell survival and migration through PI3K/AKT and MAPK/ERK pathway(Elsevier France-Editions Scientifiques Medicales Elsevier, 2018) Erdogan, Suat; Turkekul, Kader; Dibirdik, Ilker; Doganlar, Oguzhan; Doganlar, Zeynep B.; Bilir, Ayhan; Oktem, GulperiAims: To examine the functions of growth factor midkine (MK) and a flavonoid quercetin on survival, apoptosis and migration of prostate cancer (PCa) stem cells (CSCs). Main methods: CD44(+)/CD133(+) and CD44(+) stem cells were isolated from PC3 and LNCaP cells, respectively by magnetic-activated cell sorting system. 3D cell culture was used to evaluate the ability of quercetin, MK siRNA, and the combination of both to inhibit spheroid formation, apoptosis and cell cycle arrest. Image-based cytometer, RT-qPCR, Western blotting and transwell migration assays were performed. Key findings: Quercetin treatment for 24-72 h inhibited PC3 and CD44+/CD133+ stem cell proliferation in a time-and dose-dependent manner. Knockdown of endogenous MK expression significantly suppressed proliferation of CD44(+)/CD133(+) and CD44(+) cells as well as their parent cells. Co-administration of MK siRNA and quercetin reduced the cell survival, induced apoptosis and caused G1 phase cell cycle arrest more effectively than the individual therapy. Knockdown of MK significantly enhanced the inhibitory effect of quercetin on CD44(+)/CD133(+) migration and spheroid formation. In addition, the combined therapy inhibited the phosphorylation of PI3K, AKT and ERK1/2, and reduced the protein expression of p38, ABCG2 and NF-kappa B. Significance: Quercetin alone exhibited significant cytotoxic effects on CD44(+)/CD133(+). MK plays an important role in the proliferation of CD44(+)/CD133(+) and CD44(+) cells in particular, and quercetin and MK-silencing therapy may be an important strategy in targeting CSCs that play a role in relapse, migration and drug resistance.Öğe Midkine silencing enhances the anti-prostate cancer stem cell activity of the flavone apigenin: cooperation on signaling pathways regulated by ERK, p38, PTEN, PARP, and NF-?B(Springer, 2020) Erdogan, Suat; Turkekul, Kader; Dibirdik, Ilker; Doganlar, Zeynep B.; Doganlar, Oguzhan; Bilir, AyhanProstate cancer (PCa) is the most common cancer in men worldwide. Midkine (MK) is overexpressed in PCa, as well as in tumor-initiating cells termed cancer stem cells (CSCs). Apigenin is a dietary flavone with considerable anti-tumor activities. In this study, we explored the possible therapeutic use of MK silencing, apigenin treatment, and a combination of both on human PCa and prostate cancer stem cells (PCSCs). CD44(+)CD133(+) PC3 and CD44(+) LNCaP CSCs were isolated from their parent cell lines. Both MK knockdown and apigenin treatment resulted in loss of cell viability in PCSCs, and these effects were significantly elevated when apigenin was applied with MK silencing. Combined treatment of CD44(+)CD133(+) PC3 cells with apigenin and MK siRNA was also more effective in inducing apoptotic and non-apoptotic cell death when compared with individual applications. Treatment of CD44(+) LNCaP cells with apigenin significantly decreased viability, although the combination treatment did not markedly alter the individual therapy. Molecular events underlying cell cycle arrest and inhibition of the survival, proliferation, and migration of CD44(+)CD133(+) PC3 cells were found to be associated with upregulated p21, p27, Bax, Bid, caspase-3, and caspase-8 expression, as well as downregulated p-p38, p-ERK, NF-kappa B, and PARP. In addition, the combination of apigenin treatment and MK silencing showed better outcomes on the anticancer efficacy of docetaxel in CD44(+)CD133(+) PC3 cells. In conclusion, MK-regulated events are different between PCSCs, and when combined with apigenin plus MK silencing, docetaxel treatment may be a valuable approach for the eradication of PCSCs.Öğe Multifaceted impact of adipose conditioned media: Obesity-driven promotion of prostate cancer and cancer stem cell dynamics(Wiley, 2024) Erdogan, Suat; Serttas, Riza; Dibirdik, Ilker; Turkekul, KaderObesity is an established risk factor for the development and progression of prostate cancer (PC). This study used adipose conditioned media (ACM) from differentiated adipocytes to assess its effect on PC development and aggressiveness. Due to limited research on ACM's impact on isolated PC stem cells (PCSCs), we also examined CD44+ PCSCs. ACM notably boosted interleukin-1 beta (IL-1 beta), IL-6, and IL-8 production in normal prostate epithelial cells and LNCaP cells. It also increased IL-6 and IL-8 production in PC3 and CD44+ LNCaP cells, and IL-1 beta and IL-6 production in CD44+ PC3 cells. This indicates that ACM induces the production of inflammatory cytokines in both cancer and prostate epithelial cells. Furthermore, ACM promoted proliferation in androgen receptor (AR)-negative PC3 cells, CD44+ PC3 PCSCs, and nonmalignant RWPE cells, without affecting AR-positive LNCaP cells. In addition, ACM-enhanced invasion and migration potential in both PC3 and CD44+ PC3 cells. Western blot analysis indicated the involvement of NF-kappa B and AKT pathways in ACM-induced proliferation in PC3 cells and NF-kappa B in PCSCs. In ACM-treated PC3 cells, E-cadherin was downregulated, while N-cadherin, Snail, vimentin, fibronectin, and Twist were upregulated, suggesting ACM-induced invasion via classical epithelial-to-mesenchymal transition (EMT) pathways. In response to ACM, PCSCs exhibited increased expression of E-cadherin, Snail, and vimentin, which are partial EMT markers promoting stemness and resistance to apoptosis. In addition, increased expressions of Nanog, Oct3/4, survivin, and Bcl-2 were observed. Although the molecules we studied have diverse effects on cellular regulation, our data emphasize obesity's multifaceted role in promoting and aggressing PC, notably affecting PCSC populations. The link between cancer and obesity has been well-established. Excess adipocyte tissue can promote inflammation and hormone imbalances, all of which contribute to cancer development. This study investigated the effectiveness of adipose tissue secretions on different types of prostate cancer (PC) cells, the proliferation and migration of normal prostate epithelial cells. The findings revealed that adipose tissue contributed to the proliferation, invasion, and migration of PC and cancer stem cells. In addition, it showed a potential relationship between adipose tissue and the proliferation of normal prostate epithelial cells.Öğe A novel biomarker in acute cholecystitis: YKL-40(Elsevier Singapore Pte Ltd, 2023) Celikturk, Eray; Salt, Omer; Sayhan, Mustafa Burak; Dibirdik, IlkerBackground: The lack of a specific biomarker that can be used in the diagnosis of acute cholecystitis, a common cause of admission to the emergency department, delays physician efforts to diagnose and treat these patients. Therefore, the aim of this study was to measure plasma YKL-40 levels and investigate their diagnostic value in patients with acute cholecystitis (AC). Methods: This study was carried out between February 2020 and September 2020 in the adult emergency department of a tertiary university hospital. Permission was obtained from the Ethics Committee of Scientific Research on 03/02/2020 with Decision No. 03/16. The study included 80 patients who were diagnosed with acute cholecystitis and 80 healthy volunteers without known chronic diseases. Results: The median YKL-40 protein level was 798.66 pq/mL in the patient group and 392.45 pq/mL in the control group. A statistically significant difference in YKL-40 protein levels was found between the two groups. YKL-40 protein levels were significantly higher in patients diagnosed with acute cholecystitis than in healthy individuals (p < 0.001). A positive correlation was found between YKL-40 protein levels and ALT, AST, LDH, and GGT levels (r = 0.272, p = 0.015; r = 0.397, p < 0.001; r = 0.386, p < 0.001; and r = 0.264, p = 0.018; respectively). Conclusion: When evaluated together with physical examination, radiological imaging and other laboratory parameters, we think that plasma YKL-40 levels can be used effectively in the diagnosis of acute cholecystitis. (c) 2023 Asian Surgical Association and Taiwan Robotic Surgery Association. Publishing services by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/ by/4.0/).Öğe The synergistic anticancer effect of salinomycin combined with cabazitaxel in CD44+prostate cancer cells by downregulating wnt, NF-?B and AKT signaling(Springer, 2022) Erdogan, Suat; Serttas, Riza; Turkekul, Kader; Dibirdik, IlkerBackground Tumor-initiating or cancer stem cells (CSCs) reduce the effectiveness of conventional therapy. Thus, it is crucial to eliminate CSCs while killing bulky cancer cells using a combination of conventional chemotherapy and anti-CSC drugs. Salinomycin is a selective inhibitor against CSCs and shows promise in combination applications. The aim of the study was to examine the efficacy of co-administered cabazitaxel and salinomycin on the survival of prostate cancer cells and CSCs. Methods and Results CD44 + stem cells were isolated from human PC3 prostate cancer cells by using magnetic activated cell sorting. The cells were concomitantly exposed to salinomycin and cabazitaxel, and the cell survival was determined by MTT test. Apoptosis was assessed by image-based cytometer, and cell migration was evaluated by wound healing assay. The expression of target mRNA and protein were assessed by RT-qPCR and Western blot, respectively. Combination index (CI) analysis showed that simultaneous administration of salinomycin and cabazitaxel was able to exert strong synergistic effect on CD44 + subpopulation (CI = 0.33), but no synergism was observed in PC3 cells. The combination of the two agents significantly increased Bax, cytochrome c, caspase-3 and - 8 mRNA expression in CD44 + CSCs, causing apoptosis. The applied therapy strategy strongly inhibited the phosphorylation of Akt, protein expression of Akt1, NF-kappa B and Wnt. Conclusions In conclusion, our data suggest that combining salinomycin with cabazitaxel shows promise as a prostate cancer treatment approach that can target CSCs.
