Şansaçar, Merve

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https://hdl.handle.net/20.500.12573/2691
Name Variants
Sansacar, M.
Sansacar, Merve
Şansaçar, Merve
Job Title
Arş. Gör.
Email Address
merve.sansacar@agu.edu.tr
Main Affiliation
04.01. Biyomühendislik
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Current Staff
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ORCID ID
0000-0002-1731-5215
Scopus Author ID
58782858900
Turkish CoHE Profile ID
265440
Google Scholar ID
WoS Researcher ID
IZE-7343-2023

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11

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1

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8

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12

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2

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0.73

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1.09

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3

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FEBS Open Bio2
Chemistryselect1
Clinical Lymphoma Myeloma & Leukemia1
Biochemical and Biophysical Research Communications1
Journal of Experimental and Clinical Medicine (Turkey)1
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Now showing 1 - 10 of 11
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    Conference Object
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    Article
    Discovery of New Candidates Targeting the SH2 Domains of Spleen Tyrosine Kinase (Syk) Through in Silico Studies
    (Wiley-VCH Verlag GmbH, 2025) Sansacar, Merve; Sari, Ceyhun; Yucel, Muhsin Samet; Akcok, Emel Basak Gencer; Akcok, Ismail
    Src homology 2 (SH2) domains have become an increasingly popular candidate for researchers to search for novel therapeutics to target different diseases. Spleen tyrosine kinase (Syk) is one of the proteins with two SH2 domains that has a role in the pathogenesis of many diseases. Here, we report the discovery of a promising natural product (NP) inhibitor that targets the N-terminal SH2 (N-SH2) and C-terminal SH2 (C-SH2) domains of Syk simultaneously, through structure-based drug discovery approach. Molecular docking studies, followed by molecular dynamics (MD) simulations and molecular mechanics Poisson-Boltzmann surface area (MM/PBSA) calculations, were utilized to reveal the interactions between NPs from "the COlleCtion of Open NatUral producTs (COCONUT)" database and Syk enzyme. Five natural products that have lowest Scoring and Minimization with AutoDock Vina (SMINA) scores against both SH2 domains of Syk were selected for further studies and compound CNP0265345 has the best binding free energies toward both C-SH2 and N-SH2 of Syk enzyme with -44.54 and -55.98 kcal/mol, respectively. Drug-likeness properties, absorption, distribution, metabolism, and excretion (ADME) and carcinogenicity predictions were also studied. In conclusion, our work highlights a novel drug candidate to target the Syk enzyme of SH2 domains using in silico methods.
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    Article
    Efficacy of Combinatorial Inhibition of Hedgehog and Autophagy Pathways on the Survival of AML Cell Lines
    (Academic Press inc Elsevier Science, 2025) Sansacar, Merve; Pepe, Nihan Aktas; Akcok, Emel Basak Gencer; El Khatib, Mona
    Acute myeloid leukemia (AML) is a common hematopoietic disease that results from diverse genetic abnormalities. Dysregulation of important signaling pathways, including the PI3K/AKT/mTOR, Wnt and Hedgehog pathways, plays crucial roles in the development of AML. Hedgehog pathway (Hh) is a conserved signaling pathway that is crucial throughout embryogenesis. Hh plays an important role in the regulation of autophagy, known as the cellular recycling process of organelles and unwanted proteins. Many studies have noted that the modulation of autophagy could act as a survival mechanism in AML. Considering the pivotal role of autophagy and Hh signaling in AML, understanding the relationship between these pathways is important for overcoming leukemia. Therefore, we examined the efficacy of Hh inhibition by GLI-ANTagonist 61 (GANT61) in MOLM-13 and CMK cells via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenil-2H-tetrazolium bromide (MTT) cell viability assays. GANT61 resulted in decreased cell viability in both cell lines. Therefore, we focused on the outcome of autophagy modulation in AML cells. We observed that the autophagy inhibitors ammonium chloride (NH4CI), chloroquine (CQ), and nocodazole led to a significant reduction in the proliferation of both cell lines. Cotreatment with autophagy pathway inhibitors and GANT61 synergistically affected both AML cell lines. Moreover, dual targeting of these pathways resulted in arrest at the G0/G1 phase in MOLM-13 cells but not in CMK cells. Furthermore, the combination of nocodazole and GANT61 increased the expression level of LC3B-II in both cell lines. Compared with that in the untreated control cells, the GLI1 gene expression level in both cell lines was significantly lower after GANT61 and autophagy cotreatment. In conclusion, targeting Hh and autophagy could be a favorable option to combat AML.
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    Book Part
    Citation - Scopus: 1
    Measurement of Autophagic Activity in Cancer Cells With Flow Cytometric Analysis Using Cyto-Id Staining
    (Humana Press Inc., 2025) Şansaçar, Merve; Gencer Akçok, Emel Başak
    Autophagy is an evolutionarily conserved process providing the energy that cells need to survive, especially in stress situations, through catabolic processes. Considering the dual role of autophagy in cancer cells depending on the cellular context, it is crucial to comprehend the effect of drug candidates put forward to prevent cancer through the autophagy pathway. The CYTO-ID® Autophagy Detection Kit allows a rapid, specific and quantitative measurement of autophagic activity at the cellular level using a 488 nm-excitable green fluorescent detection reagent via flow cytometer. In this chapter, we present the CYTO-ID® Autophagy Detection method with a stepwise protocol to monitor the autophagy flux after the application of any compound to suspension cancer cell lines with flow cytometric analysis. © 2025 Elsevier B.V., All rights reserved.
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    Conference Object
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    Master Thesis
    Otofaji Modülasyonu ve Hedgehog İnhibisyonunun AML Hücre Hatlarının Çoğalması ve Hayatta Kalması Üzerine Etkisi
    (2019) ŞANSAÇAR, MERVE; Şansaçar, Merve; Khatıb, Mona El
    Akut miyeloid lösemi (AML), translokasyon, delesyon veya insersiyon gibi birçok kromozomal anormallik içeren ve hematopoetik malignite ile sonuçlanan heterojen bir hastalıktır. PI3K / AKT / mTOR, Notch ve Hedgehog yolağı gibi sinyal yollarındaki bozulmalar AML patogenezinde rol oynar. Hedgehog yolağı (Hh) embriyogenez sırasında önemli olan korunmuş bir sinyal yolağıdır. Diğer yolaklarla etkileşime girer ve hücresel bir bozulma ve organel yıkım sürecini oluşturan otofajiyi düzenler. Bazı çalışmalar, otofaji modülasyonunun AML' de bir kaçış mekanizması olarak işlev görebileceğini öne sürmüştür. AML'de otofaji ve Hh rolü göz önüne alındığında, lösemik büyümenin üstesinden gelmek için otofaji ve Hh yolu arasındaki ilişkiyi anlamak önemlidir. Dolayısıyla, GANT61 ile Hh inhibisyonunun AML hücre hatları üzerindeki etkisini MTT hücre canlılığı tahlili kullanarak kontrol ettik. GANT61, AML hücre hatlarında bir azalmaya yol açtı. Bundan sonra, otofaji modülasyonunun AML hücre hatları üzerindeki etkisini anlamaya çalıştık ve otofaji inhibitörleri, NH4CI, Chloroquine (CQ), Hydroxychloroquine ve Nocodazole'ün CMK ve MOLM-13 hücre hatlarının çoğalmasında bir azalmaya yol açtığını gördük. Bununla birlikte, bir otofaji aktivatörü olan PP242, AML hücre hatlarının çoğalmasına etki etmedi. Otofaji modülatörlerinin ve GANT61'in kombinasyon tedavisi, MOLM-13 üzerinde sinerjistik bir etkiye sahipti fakat CMK üzerinde değildi. GANT61 tedavisi, AML hücre hatlarında, western blotlama ile tespit edilen LC3II'nin ekspresyonunda bir artışla ilişkili olan otofajiyi arttırmıştır. Ayrıca, nodadazole ve GANT61 ile kombinasyon tedavisi, hem MOLM-13 hem de CMK hücre hatlarında LC3B-II'de artan bir artış göstermiştir. AKT protein ekspresyonu, tedavi tipine ve hücre hattına bağlı olarak değişti. Sonuç olarak Hh ve otofajinin hedeflenmesi, MOLM-13 hücre hattına karşı umut verici bir tedavidir ancak CMK'ya karşı değildir. Anahtar kelimeler: Akut miyeloid lösemi, Hedgehog yolağı, Otofaji
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    Conference Object
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    Article
    Citation - Scopus: 1
    Targeting HDAC Enzymes by SAHA Enhances the Cytotoxic Effects of Cisplatin on Acute Myeloid Leukemia Cells
    (Ondokuz Mayis Universitesi, 2024) Şansaçar, Merve; Pekin, Özge; Gencer Akçok, Emel Başak
    Chemotherapy is a widely used therapeutic approach to combat hematopoietic malignancies such as acute myeloid leukemia (AML). Although cisplatin is known as the first-generation platinum-based chemotherapy inhibitor, the wide use of cisplatin eventually leads to drug resistance, which is the biggest impediment to cancer chemotherapy. Histone deacetylase enzyme (HDAC) inhibitors have the ability to induce cell cycle arrest and apoptosis in different types of cancer, which stands as a promising alternative for those cancer patients not appropriate for intensive chemotherapy. This study concluded that there was a significant decrease in the proliferation of MOLM-13 and MV4-11 FLT3-ITD+ AML cell lines with the increasing SAHA and cisplatin concentrations in 48 hours using MTT cell proliferation assay. Moreover, the combination of SAHA and cisplatin led to a reduction in the proliferation of both cell lines correlated with the synergistic effect of the two drugs depending on the combination index (CI). Furthermore, investigating apoptosis for combined administration resulted in increased induction of apoptosis by Annexin-V/PI double staining. In conclusion, although additional studies are needed to fully elucidate the molecular mechanism underlying this combination, we propose a new approach to targeting AML, as AML increases over time with drug resistance and the consequent year-on-year increase in patient mortality. © 2025 Elsevier B.V., All rights reserved.
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    Article
    Citation - WoS: 8
    Citation - Scopus: 10
    Inhibition of PI3K-AKT-mTOR Pathway and Modulation of Histone Deacetylase Enzymes Reduce the Growth of Acute Myeloid Leukemia Cells
    (Humana Press inc, 2023) Sansacar, Merve; Sagir, Helin; Akcok, Emel Basak Gencer
    One of the most widespread forms of blood cancer is known as acute myeloid leukemia (AML) which has an incidence of 80% with poor prognosis. Although there are different treatment methods for AML in clinic, the heterogeneity and complexity of the disease show that new treatments are needed. The aim of this study is to investigate the anticancer effects of inhibition of PI3K and HDAC enzymes on CMK and MOLM-13 AML cells lines. We demonstrated that the combination of LY294002 with SAHA and Tubastatin A significantly decreased the cell viability of both cell lines. In contrast, the LY294002 and PCI-34051 combination did not show a significant difference compared to the single LY294002 administration. The combination treatment of LY294002 and HDAC inhibitors did not induce apoptosis significantly. However, LY294002 + SAHA and LY294002 + PCI-34051 resulted in G0/G1 and G2/M cell cycle arrest in CMK cells, respectively. On the other hand, compared to control cells, LY294002 + SAHA and LY294002 + PCI-34051 led to G0/G1 phase arrest in MOLM-13. Furthermore, the LY294002 + PCI-34051 combination elevated the expression rate of LC3BII/I, an autophagy marker, in CMK cells by 2.5-fold. Our study revealed that the combinations of PI3K inhibitor and HDAC inhibitors showed a synergistic effect and caused a reduction in cell viability and increased cell cycle arrest on MOLM-13 and CMK cell lines. In addition, the expression of LC3BII was elevated in the CMK cell line. In conclusion, although more mechanistic studies are required, a combinational inhibition of PI3K and HDAC could be a promising approach for AML.
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    Research Project
    Pi3k-Akt-Mtor Yolağı Ve Histon Deasetilaz Enzimlerinin Hedeflenmesinin Akut Myeloid Lösemi Hücreleri Üzerine Antitümör Etkisinin Incelenmesi
    (TÜBİTAK, 2022) Gencer Akçok, Emel Başak; Şansaçar, Merve; Karaca, Münevver; Okur, Tuğba
    Akut Miyeloid Lösemi (AML), periferik kan, kemik iliği, dalak ve karaciğerde blast adı verilen_x000D_ olgunlaşmamış miyeloid hücrelerin birikmesiyle karakterize edilen ve sonunda hematopoietik_x000D_ maligniteye yol açan bir hastalıktır. Genetik anormalliklerin yanı sıra PI3K/AKT/mTOR, Wnt,_x000D_ Notch, STAT3, Hedgehog gibi önemli hücresel yolakların AML patogenezinde rol oynadığı_x000D_ bildirilmiştir. Histon deasetilaz (HDAC) inhibitörleri, AML için umut verici antikanser aktiviteye_x000D_ sahiptir. Çalışmada, PI3K/AKT/mTOR yolunun inhibisyonunun ve HDAC inhibisyonunun farklı_x000D_ AML alt gruplarının hücre hatları olan MOLM-13 ve CMK hücre hatları kullanılarak bu_x000D_ hastalığın altında yatan moleküler mekanizma üzerindeki etkisinin araştırılması amaçlamıştır._x000D_ Bu amaçla PI3K inhibitörü LY294002 ve HDAC inhibitörleri (SAHA, PCI-3501 ve Tubastatin A)_x000D_ ve bunların kombinasyonlarının etkisi incelenmiştir. Hücre proliferasyonu MTT hücre_x000D_ sitotoksisite testi ile apoptoz oranları ise Annexin-V/PI çift boyama yöntemi ile belirlenmiş,_x000D_ ilaçların hücre döngüsüne olan etkileri de PI boyaması ile belirlenmiştir. Otofaji belirteci olan_x000D_ LC3B protein seviyesi moleküler düzeyde western blot ile doğrulanmıştır._x000D_ Kullanılan inhibitörler her iki hücre hattı üzerinde düşük mikromolar konsantrasyonda hücre_x000D_ canlılığını azaltmıştır. Sonuçlar LY294002+SAHA kombinasyon tedavisinin MOLM-13_x000D_ hücrelerinde hücre proliferasyonunu %50, CMK hücrelerinde ise %25 azalma gösterdiği_x000D_ belirlenmiştir. LY294002+Tubastatin A tedavisi, MOLM-13 ve CMK hücrelerinde hücre_x000D_ proliferasyonunu sırasıyla %65 ve %40 oranında azalttığını göstermiştir. Sonuçlarımız,_x000D_ LY294002 ve HDAC inhibitör kombinasyonlarının kontrol hücrelerine kıyasla MOLM-13_x000D_ hücrelerinde G1 fazı tutuklanmasıyla sonuçlandığını gösterdi. Öte yandan, LY294002+SAHA,_x000D_ LY294002+PCI-3501 ve LY294002+Tubastatin A kombinasyonları ile tedavi edilen CMK_x000D_ hücreleri, sırasıyla G2/M, G2/M ve G1 fazında tutuklanmıştır. Kombinasyonların apoptotik_x000D_ hücre ölümü üzerine etkisine bakılmış, LC3BII/I protein ifade düzeyi kombinasyon tedavisi_x000D_ sonucunda incelenmiştir._x000D_ HDAC enzimlerinin hem AML hem de farklı kanserler üzerindeki etkileri düşünüldüğünde,_x000D_ HDAC inhibisyonu AML için önemli ve yüksek potansiyelli bir hedeftir. Bu nedenle_x000D_ PI3K/AKT/mTOR yolağı ve HDAC'lerin farklı alt gruplarda inhibisyonunun araştırılması,_x000D_ AML'nin patogenezine yol açan mekanizmalar hakkında fikir verebilir. Sonuç olarak,_x000D_ PI3K/AKT/mTOR ve HDAC'nin bu inhibisyonunun, AML'nin ortadan kaldırılmasıyla_x000D_ sonuçlanan daha spesifik bir kombinasyon hedefli tedaviye yol açacağı umulmaktadır.