Cengiz Tuncer

Dr. Cengiz Tuncer

orcid

Research Focus & Metrics

Academic Career Length

8Years (2019-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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29 March 2023 in Environmental Toxicology
Verified
Journal Article
Closed access
CHCeyhan Hacıoğlu
Ceyhan Hacıoğlu
FATİH KARFATİH KAR
FATİH KAR
FDFatih Davran
Fatih Davran
CTCengiz Tuncer
Cengiz Tuncer

30 March 2025 in Journal of Cellular and Molecular Medicine
Verified
Journal Article
Open access
GKGüven Kilic
Güven Kilic
CHCeyhan Hacıoğlu
Ceyhan Hacıoğlu
CTCengiz Tuncer
Cengiz Tuncer
EKEzgi Kar
Ezgi Kar
FATİH KARFATİH KAR
FATİH KAR
CECigdem Erdin
Cigdem Erdin
Ferroptosis, a distinct form of regulated cell death, plays a role in glioma pathogenesis. SRY‐box (SOX) transcription factors are key regulators of cancer progression. In this study, we investigated the role of SOX10 in ferroptosis induction in U87 cells following boric acid treatment. First, the cytotoxic effects of boric acid on HMC3 and U87 cells were assessed using CCK8 and BrdU incorporation assays. Subsequently, SOX10, GPX4, ACSL4, GSH, MDA, total ROS, Fe 2+ , and TFR levels were analysed using ELISA, Western blot, and RT‐PCR techniques. Additionally, DAPI staining was performed to evaluate nuclear abnormalities. According to the CCK8 analysis, the IC50 value for boric acid was determined to be 3.12 mM for HMC3 cells and 532 μM for U87 cells, a finding further supported by BrdU incorporation analysis, which indicated that U87 cells were more sensitive to boric acid. Western blot and RT‐PCR analyses revealed that SOX10 expression was significantly higher in U87 cells compared to HMC3 cells. Boric acid treatment led to a reduction in GSH, GPX4, and SOX10 levels in U87 cells, while inducing an increase in MDA, total ROS, ACSL4, Fe 2+ , and TFR levels. Moreover, microscopic analysis demonstrated that boric acid treatment induced both morphological and nuclear abnormalities in U87 cells. In conclusion, our findings demonstrate that SOX10 is involved in the ferroptosis signalling pathway and that boric acid effectively suppresses U87 cell viability by targeting the SOX10/GPX4/ACSL4 axis.

18 March 2025 in Journal of Cellular and Molecular Medicine
Verified
Journal Article
Open access
CTCengiz Tuncer
Cengiz Tuncer
CHCeyhan Hacıoğlu
Ceyhan Hacıoğlu
The development of resistance to chemotherapy in the case of aggressive glioblastoma multiforme (GBM) presents a significant treatment challenge. Dysregulation of the Notch signalling pathway promotes tumour proliferation in GBM cells. This study was that targeting the Notch signalling pathway could be a potential therapeutic approach for GBM. Initially, temozolomide‐(TMZ)‐resistant GBM cells were generated, and the effect of Notch1 on the expression of multiple resistance proteins within these cells was investigated. Subsequently, the expression of Notch‐1 in GBM cells was reduced using siRNA. Results revealed a significant reduction in TMZ sensitivity in TMZ‐resistant GBM cells, accompanied by a substantial increase in the expression of major vault protein‐(MVP), O6‐methylguanine‐DNA‐methyltransferase‐(MGMT), and ATP‐binding‐cassette transporter‐G2‐(ABCG2). Furthermore, TMZ‐resistant U87‐R and U251‐R cells exhibited higher proliferation rates compared to their parental control cells (U87 and U251). Additionally, we observed that downregulating Notch‐1 signalling inhibited the proliferation of TMZ‐resistant U87‐R and U251‐R cells. This downregulation led to the inactivation of MGMT, ABCG2, and MVP. Importantly, it increased chemosensitivity to TMZ, particularly by downregulating MVP expression. Consequently, Notch1 could serve as a potential therapeutic target for GBM cells and may be effective in preventing TMZ resistance by targeting MVP, as well as MGMT and ABCG2 in GBM cells.

3 November 2025 in Metabolic Brain Disease
Verified
Journal Article
Closed access
PDF file
MKMustafa Kilic
Mustafa Kilic
CHCeyhan Hacıoğlu
Ceyhan Hacıoğlu
STSibel Tuncer
Sibel Tuncer
ATAhmet Taskesen
Ahmet Taskesen
CTCengiz Tuncer
Cengiz Tuncer

20 October 2023 in Konuralp Tip Dergisi
Verified
Journal Article
Closed access
EŞERDINÇ ŞENGÜLDÜR
ERDINÇ ŞENGÜLDÜR
KSKudret Selki
Kudret Selki
CTCengiz Tuncer
Cengiz Tuncer
MDMehmet Cihat Demir
Mehmet Cihat Demir
Objective: To reveal the characteristics of patients needing neurosurgery by examining neurosurgery consultations within the emergency department (ED) admissions of a tertiary academic hospital. Method: This is a retrospective, single-centre observational study. Patients admitted to the ED between 01.01.2022 and 31.12.2022 and consulted to the neurosurgery department were identified through the hospital computer system and included in the study. The demographic information of the patients, mode of admission to the ED, the reasons for admission, the time of admission, the number of brain computed tomography (CT) scans, whether they underwent surgery or not, and the mortality results were recorded. Results: A total of 441 neurosurgery consultations were examined. Fall 35.6% (n=157) and traffic accident 16.6% (n=73) were the most common reasons for consultation. It was observed that 92.5% (n=408) of the patients had a brain CT scan, and 19.5% (n=86) had two or more brain CTs. It was determined that 12.7% (n=56) of the patients consulted for neurosurgery were operated on, and 4.1% (n=18) of the patients' hospital admissions resulted in death. Only 53.7% (n=237) of the patients who underwent neurosurgery consultation were discharged from the ED. It was determined that significantly more Neurosurgery consultations were requested during working hours (p = 0.013) Conclusion: Most consultation calls from the ED to neurosurgery are for trauma patients. Brain CT examination is frequently used in neurosurgical patient evaluation. As a result of the consultations, almost half of the patients are hospitalized. Emergency physicians can select patients who need neurosurgery well.

1 October 2019 in Journal of Turkish Spinal Surgery
Verified
Journal Article
Closed access
CTCengiz Tuncer
Cengiz Tuncer
ÖPÖmer Polat
Ömer Polat
UEUygur Er
Uygur Er