Kılıç, Nedret

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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
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID

Sustainable Development Goals

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

42

Citations

521

h-index

12

Documents

38

Citations

482

Scholarly Output

5

Articles

4

Views / Downloads

6/0

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
Current Page: 1 / 1

Scopus Quartile Distribution

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Scholarly Output Search Results

Now showing 1 - 3 of 3
  • 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.
  • 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.