Kılıç, Nedret

Profile Picture
Profile URL
https://hdl.handle.net/20.500.14411/6669
Name Variants
Kılıç, Nedret
K., Nedret
Kılıç,N.
Nedret, Kılıç
N., Kılıç
Kilic, Nedret
N.,Kilic
Nedret Kılıç
Kilic,N.
Kiliç N.
Kilic N.
Kilic,Nedret
N., Kilic
Nedret, Kilic
Kılıç N.
N.,Kılıç
K.,Nedret
Kılıc N.
KŞişl.c N.
Job Title
Profesör Doktor
Email Address
nedret.kilic@atilim.edu.tr
Main Affiliation
Basic Sciences
Status
Website
https://www.atilim.edu.tr/home/
ORCID ID
0000-0002-5747-9433
Scopus Author ID
7005266569
Turkish CoHE Profile ID
3281
Google Scholar ID
WoS Researcher ID
AAK-5395-2021

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
Research Products
ZERO HUNGER2
ZERO HUNGER
0
Research Products
GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
4
Research Products
QUALITY EDUCATION4
QUALITY EDUCATION
0
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GENDER EQUALITY5
GENDER EQUALITY
0
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
0
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
1
Research Products
DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
Research Products
INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
0
Research Products
REDUCED INEQUALITIES10
REDUCED INEQUALITIES
0
Research Products
SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
Research Products
RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
Research Products
CLIMATE ACTION13
CLIMATE ACTION
0
Research Products
LIFE BELOW WATER14
LIFE BELOW WATER
0
Research Products
LIFE ON LAND15
LIFE ON LAND
0
Research Products
PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
0
Research Products
PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
0
Research Products
Documents

42

Citations

521

h-index

12

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Documents

38

Citations

482

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Scholarly Output

5

Articles

4

Views / Downloads

23/131

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

8

Scopus Citation Count

9

Patents

0

Projects

0

WoS Citations per Publication

1.60

Scopus Citations per Publication

1.80

Open Access Source

3

Supervised Theses

0

JournalCount
Annals of Surgical Oncology1
Celal Bayar Üniversitesi Sağlık Bilimleri Enstitüsü Dergisi1
International Journal of Pharmaceutics1
Scientific Reports1
World Neurosurgery1
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Start date: 2017

Scholarly Output Search Results

Now showing 1 - 5 of 5
  • Thumbnail Image
    Letter
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    Article
    İntrakranial Tümörlerde Klk5, Klk6 ve Klk7 Ekspresyonlarının Araştırılması
    (2020) Turna, Gamze; Kılıç, Nedret; Kurt, Gökhan; Doğulu, Fikret; Ceviker, Necdet; Saltoğlu, Gamze Turna
    Giriş ve Amaç: 19. kromozom (19q13.3-4) üzerinde bulunan 15 genden oluşan kallikrein ilişkili peptidazlar(KLK’lar), serin proteazların bir alt grubudur. Daha önce yapılan bazı çalışmalar KLK'ların çeşitli kanser türleriyleilişkili olduğunu göstermiştir. Bununla birlikte, intrakranial tümörlerde KLK'ların tanı ve prognozdaki rolünüaraştıran az sayıda çalışma bulunmaktadır. Bu nedenle, bu çalışmada intrakranial tümörlerde KLK5, KLK6 veKLK7'nin ekspresyon düzeylerindeki değişimlerin belirlenmesi amaçlamıştır.Gereç ve Yöntemler: Menenjiom grade I (n = 15) ve glioblastoma multiforme (n = 15) tümör örneklerinde, KLK5,KLK6 ve KLK7 mRNA ekspresyon düzeyleri ters transkriptaz polimeraz zincir reaksiyonu (RT-PCR) kullanılaraktespit edildi. Protein ekspresyonları ise western blotting yöntemi kullanılarak belirlendi.Bulgular: KLK5 ve KLK7’nin mRNA ve proteinleri menenjiom grubunda daha sıklıkla ifade edilirken, KLK6’nınmRNA ve proteini glioblastoma grubunda daha sıklıkla ifade edilmektedir.Sonuç: Menenjiom ve glioblastoma grupları karşılaştırıldığında KLK5, KLK6 ve KLK7 mRNA ve proteinekspresyon düzeylerinde farklılıklar olduğu tespit edilmiştir. Bu genler intrakranial tümörlerin tanısı için yeni birbiyobelirteç olma potansiyeline sahip olabilir
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    Article
    ACPA Prevents Lung Fibroblast-to Transformation by Reprogramming the Tumor Microenvironment through NSCLC-Derived Exosomes
    (Nature Portfolio, 2025) Boyacioglu, Ozge; Kalali, Berfin Deniz; Recber, Tuba; Gelen-Gungor, Dilek; Nemutlu, Emirhan; Eroglu, Ipek; Korkusuz, Petek; Kilic, Nedret
    Non-small cell lung cancer (NSCLC) accounts for most lung cancer cases. Current treatments often cause systemic side effects or lead to drug resistance, prompting the development of new therapies targeting tumors and related cells simultaneously. Cancer-associated fibroblasts (CAFs) are crucial stromal cells within the tumor microenvironment (TME), making them potential targets for therapy. Previously, we found that the CB1 receptor agonist ACPA has anti-tumor effects on NSCLC, inhibiting pathways such as Akt/PI3K, JNK, glycolysis, the citric acid cycle, and the urea cycle both in vitro and in vivo. We hypothesize that ACPA could enhance therapy by inhibiting the transformation of lung fibroblasts into CAFs via exosomes. Control and ACPA-treated NSCLC cell exosomes exhibited similar size, PDI, ZP, and high expression of CD9, CD63, and CD81. ACPA-treated exosomes showed reduced levels of miR-21 and miR-23. These exosomes decreased fibroblast viability within 12 h by disrupting pentose phosphate, lipid, and amino acid metabolism, and by lowering PDPN, alpha-SMA, and FAP expressions. This research highlights ACPA as a promising chemotherapeutic agent, capable of improving NSCLC treatment and reprogramming the TME with more targeted therapies.
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    Article
    Citation - WoS: 3
    Citation - Scopus: 4
    A Novel Injectable Nanotherapeutic Platform Increasing the Bioavailability and Anti-Tumor Efficacy of Arachidonylcyclopropylamide on an Ectopic Non-Small Cell Lung Cancer Xenograft Model: A Randomized Controlled Trial
    (Elsevier, 2025) Boyacioglu, Ozge; Varan, Cem; Bilensoy, Erem; Aykut, Zaliha Gamze; Recber, Tuba; Nemutlu, Emirhan; Korkusuz, Petek
    Rapid progressing non-small cell lung adenocarcinoma (NSCLC) decreases treatment success. Cannabinoids emerge as drug candidates for NSCLC due to their anti-tumoral capabilities. We previously reported the controlled release of Arachidonylcyclopropylamide (ACPA) selectively targeting cannabinoid 1 (CB1) receptor in NSCLC cells in vitro. Hydrophobic polymers like polycaprolactone (PCL) offer prolonged circulation time and slower drug clearance which is suitable for hydrophobic molecules like ACPA. Thus, the extended circulation time with enhanced bioavailability and half-life of nanoparticular ACPA is crucial for its therapeutic performance in the tumor area. We assumed that a novel high technology-controlled release system increasing the bioavailability of ACPA compared to free ACPA could be transferred to the clinic when validated in vivo. Plasma profile of ACPA and ACPA-loaded PCL-based nanomedicine by LC-MS/MS and complete blood count (CBC) was assessed in wild-type Balb/c mice. Tumor growth in nanomedicine-applied NSCLC-induced athymic nude mice was assessed using bioluminescence imaging (BLI) and caliper measurements, histomorphometry,immunohistochemistry, TUNEL assay, and Western blot on days 7-21. Injectable NanoACPA increased its systemic exposure to tissues 5.5 times and maximum plasma concentration 6 times higher than free ACPA by substantially improving bioavailability. The potent effect of NanoACPA lasted for at least two days on ectopic NSCLC model through Akt/PI3K, Ras/MEK/Erk, and JNK pathways that diminished Ki-67 proliferative and promoted TUNEL apoptotic cell scores on days 7-21. The output reveals that NanoACPA platform could be a chemotherapeutic for NSCLC in the clinic following scale-up GLP/GMP-based phase trials, owing to therapeutic efficacy at a safe low dose window.
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    Article
    Citation - WoS: 5
    Citation - Scopus: 5
    Thioredoxin System and Mir-21, Mir-23a/B and Let-7a as Potential Biomarkers for Brain Tumor Progression: Preliminary Case Data
    (Elsevier Science inc, 2022) Kilic, Nedret; Boyacioglu, Ozge; Saltoglu, Gamze Turna; Bulduk, Erkut Baha; Kurt, Gokhan; Korkusuz, Petek
    BACKGROUND: The thioredoxin system and microRNAs (miRNAs) are potential targets for both cancer progression and treatment. However, the role of miRNAs and their relation with the expression profile of thioredoxin system in brain tumor progression remains unclear. METHODS: In this study, we aimed to determine the expression profiles of redox components Trx-1, TrxR-1 and PRDX-1, and oncogenic miR-21, miR-23a/b and let-7a and oncosuppressor miR-125 in different brain tumor tissues and their association with increasing tumor grade. We studied Trx-1, TrxR-1, and PRDX-1 messenger RNA expression levels by quantitative real-time polymerase chain reaction and protein levels by Western blot and miR-23a, miR-23b, miR-125a, miR-21, and let-7a miRNA expression levels by quantitative real-time polymerase chain reaction in 16 glioma, 15 meningioma, 5 metastatic, and 2 benign tumor samples. We also examined Trx-1, TrxR-1, and PRDX-1 protein levels in serum samples of 36 patients with brain tumor and 37 healthy volunteers by enzyme-linked immunosorbent assay. RESULTS: We found that Trx-1, TrxR-1, and PRDX-1 presented high messenger RNA expression but low protein expression in low-grade brain tumor tissues, whereas they showed higher protein expression in sera of patients with low-grade brain tumors. miR-23b, miR-21, miR-23a, and let-7a were highly expressed in low-grade brain tumor tissues and positively correlated with the increase in thioredoxin system activity. CONCLUSIONS: Our findings showed that Trx-1, TrxR-1, miR-21, miR-23a/b, and let-7a might be used for brain tumor diagnosis in the clinic. Further prospective studies including molecular pathway analyses are required to validate the miRNA/Trx system regulatory axis in brain tumor progression.