Pelin Balcik-Ercin
@biyoloji.deu.edu.tr
faculty of science, department of biology
Dokuz Eylul University
EDUCATION
PhD, Molecular Biology and Genetics, Gebze Technical University
RESEARCH, TEACHING, or OTHER INTERESTS
Biochemistry, Genetics and Molecular Biology, Cell Biology, Cancer Research
Scopus Publications
Scopus Publications
Pelin Balcik-Ercin, Gülçin Ekineker, Nazlı Salik, Bahar Aydoğdu, Tamer Yagci, and Meltem Göksel
Elsevier BV
Pelin Balcik-Ercin, , Arzu Aysan, Nazli Salik, Esma Erciyas, , , , and
AVES YAYINCILIK A.Ş.
BACKGROUND/AIMS
Sine oculis homeoprotein 1 exerts an essential role in embryonic development, and it was also identified to be reactivated in various types of mammalian cancer. The sine oculis homeoprotein 1 transcription factor was demonstrated to induce epithelial-mesenchymal transition, regulate crucial genes associated with cancer progression, and increase the oncogenic potential of cells. Therefore, the present study aimed to identify the role of sine oculis homeoprotein 1 in cancer.
MATERIALS AND METHODS
Sine oculis homeoprotein 1 gene expression was tested with real-time quantitative polymerase chain reaction (PCR) in different cancer types. Sine oculis homeoprotein 1 expression was suppressed by short hairpin RNA transduction in the SNU398 hepatocellular carcinoma cell line. The effects of sine oculis homeoprotein 1 on cell proliferation, drug resistance, and sphere formation were assessed in shSIX1 cells. Immunohistochemical and in silico analyses were performed to determine the prognostic role of sine oculis homeoprotein 1 expression.
RESULTS
The upregulated expression levels of sine oculis homeoprotein 1 were revealed to be correlated with the stage of the disease in breast, colon, and liver cancer, with liver cancer exhibiting the highest expression profile. Sine oculis homeoprotein 1 downregulation significantly affected cell proliferation and suppressed sorafenib resistance and sphere-forming ability. Furthermore, sine oculis homeoprotein 1 knockdown cells were identified to have decreased CD90 levels, essential for cancer stem cell properties. Finally, sine oculis homeoprotein 1 expression was a CD90-independent biomarker for the clinical prognosis of liver cancer.
CONCLUSION
The results of this study showed that the knockdown of sine oculis homeoprotein 1 expression might help to prevent hepatocarcinogenesis by increasing drug sensitivity and controlling tumor sphere formation. Overall, these results indicated that sine oculis homeoprotein 1 expression might be useful as a diagnostic marker for patients with hepatocellular carcinoma.
Pelin Balcik-Ercin and Belgin Sever
Elsevier BV
Pelin Balcik-Ercin
Bangladesh Journals Online (JOL)
The present study was designed to explore phlorotannin eckol protein targets and evaluate the anti-cancer effects of eckol against human breast cancer cells. ProTox-II server and protein-ligand docking analysis deter-mined the aryl hydrocarbon receptor (AhR) as a putative target of eckol. The AhR has been determined as a potential target for breast cancer treatment. The effect of eckol treatment on proliferation, apoptosis, and cell cycle activities was detected in MDA-MB-231 and SK-BR-3 breast cancer cell lines which were selected dependent on AhR expression profiles. Consistent with the AhR expression profile, MDA-MB-231 cells were more sensitive to eckol treatment compared to SK-BR-3 cells in proliferation, apoptosis and cell cycle results. Eckol treatment shows a significant antiproliferative and apoptotic response in breast cancer cells. Overall, these results indicated that the action of eckol may be related to the AhR gene regulation in different breast cancer cell lines.
Özge Eroğlu Gülümsek, Esma Erciyas Baykal, Cansu Küçükpolat, Emel Önal, Pelin Balcik-Ercin, Tamer Yagci, Vefa Ahsen, and Ayşe Gül Gürek
Informa UK Limited
Abstract N,N′-bis(aniline)glyoxime (H2L, 1) has been prepared from aniline and (E,E)-dichloroglyoxime (DCGO) or (E,E)-dibromoglyoxime (DBGO). The reaction of N,N′-bis(aniline)glyoxime (H2L, 1) with solution of PtCl2 in dimethylsulfoxide produced brown-colored bis(E,E-dioximato)platinum(II) complex {[(E,E)-Pt(HL)2]} (1a) featuring N-chelating ligand. The crystal structure of this complex has been identified by X-ray diffraction on a single-crystal. In vitro assay of proliferation, cell death, DNA-damage and cell uptake activities of 1 and 1a were tested in HCC cell lines, SNU-182 and HUH-7. 1a has an anti-proliferative effect in HCC cells, however, 1 did not. Furthermore, the cellular uptake of 1a was relatively high compared to cisplatin cellular platinum levels. Compatible with proliferation and cellular uptake results, treatment with 1a caused DNA-damage and subsequent apoptosis in both HCC cell lines.
Pelin Balcik-Ercin, Laure Cayrefourcq, Rama Soundararajan, Sendurai A. Mani, and Catherine Alix-Panabières
MDPI AG
Metastasis is a complicated and only partially understood multi-step process of cancer progression. A subset of cancer cells that can leave the primary tumor, intravasate, and circulate to reach distant organs are called circulating tumor cells (CTCs). Multiple lines of evidence suggest that in metastatic cancer cells, epithelial and mesenchymal markers are co-expressed to facilitate the cells’ ability to go back and forth between cellular states. This feature is called epithelial-to-mesenchymal plasticity (EMP). CTCs represent a unique source to understand the EMP features in metastatic cascade biology. Our group previously established and characterized nine serial CTC lines from a patient with metastatic colon cancer. Here, we assessed the expression of markers involved in epithelial–mesenchymal (EMT) and mesenchymal–epithelial (MET) transition in these unique CTC lines, to define their EMP profile. We found that the oncogenes MYC and ezrin were expressed by all CTC lines, but not SIX1, one of their common regulators (also an EMT inducer). Moreover, the MET activator GRHL2 and its putative targets were strongly expressed in all CTC lines, revealing their plasticity in favor of an increased MET state that promotes metastasis formation.
Kevser Harmandar, Mehmet F. Saglam, Ibrahim F. Sengul, Gülçin Ekineker, Pelin Balcik-Ercin, Meltem Göksel, and Devrim Atilla
Elsevier BV
Pelin Balçik-Erçin, Metin Çetin, Meltem Göksel, and Mahmut Durmuş
Royal Society of Chemistry (RSC)
In this study, the peripherally biotin-substituted zinc(ii) phthalocyanine (Pc2) was synthesized as a photosensitizer for the treatment of cancer by photodynamic therapy.
P. Balcik-Ercin, M. Cetin, I. Yalim-Camci, T. Uygur, and T. Yagci
The Russian Academy of Sciences
Irem Yalim‐Camci, Pelin Balcik‐Ercin, Metin Cetin, Gorkem Odabas, Nurettin Tokay, A. Emre Sayan, and Tamer Yagci
Wiley
Epithelial‐mesenchymal transition (EMT) is an embryonic program that is reactivated in cancer and regulates the invasion and metastasis of tumor cells. Zinc finger E‐box binding homeobox 2 (ZEB2) induces EMT by upregulating matrix metalloproteinases (MMP), yet MMP genes lack ZEB2 binding motif in their promoters. Recently, expression of MMPs was associated to the activation of ETS1 transcription factor; however, a link between ZEB2 and ETS proto‐oncogene 1, transcription factor (ETS1) remains to be elucidated. Hence, we investigated the transcriptional regulation of ETS1 by ZEB2 after our initial observation that ZEB2 and ETS1 are coexpressed in hepatocellular carcinoma cells (HCCs). Chromatin immunoprecipitation and luciferase reporter assays clearly showed that ZEB2 binds to E‐box sequences on the promoter of ETS1. Elevated expression of ETS1 was found in DLD‐ZEB2 and A431‐ZEB2 inducible systems, and knockdown of ZEB2 caused an explicit downregulation of ETS1 in shZEB2‐SNU398 and shZEB2‐SK‐HEP‐1 cells. Repression of ETS1 expression in ZEB2‐induced conditions substantially impaired the migration and invasive capacities of DLD1 cells. Mechanistically, knockdown of ETS1 in ZEB2‐expressing cells resulted in the downregulation of established ZEB2 targets TWIST and MMP9. Correlation analyses in HCC lines, cancer complementary DNA arrays, and The Cancer Genome Atlas RNA‐sequencing data set revealed that ZEB2 and ETS1 are coexpressed, and their expressions in human tumors show a highly significant positive correlation. Our results demonstrated that ZEB2 acts as an upstream regulator of ETS1 and, in turn, ETS1 maintains ZEB2‐induced EMT. These findings add another level of complexity to the understanding of ZEB2 in the invasion and metastasis of cancer cells, and put ZEB2/ETS1 axis as a novel therapeutic target in human malignancies.
Metin Cetin, Gorkem Odabas, Leon Douglas, Patrick Duriez, Pelin Balcik-Ercin, Irem Yalim-Camci, Abdulkadir Sayan, and Tamer Yagci
MDPI AG
Background: Hepatocellular carcinoma (HCC) is a common and deadly cancer; however, very little improvement has been made towards its diagnosis and prognosis. The expression and functional contribution of the receptor tyrosine kinase ROR1 have not been investigated in HCC before. Hence, we investigated the expression of ROR1 in HCC cells and assessed its involvement in hepatocarcinogenesis. Methods: Recombinant bacterial ROR1 protein was used as an immunogen to generate ROR1 monoclonal antibodies. ROR1 transcript levels were detected by RT-qPCR and the protein expression of ROR1 in HCC was assessed by Western blotting by using homemade anti-ROR1 monoclonal antibodies. Apoptosis, cell cycle, trans-well migration, and drug efflux assays were performed in shRNA-ROR1 HCC cell clones to uncover the functional contribution of ROR1 to hepatocarcinogenesis. Results: New ROR1 antibodies specifically detected endogenous ROR1 protein in human and mouse HCC cell lines. ROR1-knockdown resulted in decreased proliferation and migration but enhanced resistance to apoptosis and anoikis. The observed chemotherapy-resistant phenotype of ROR1-knockdown cells was due to enhanced drug efflux and increased expression of multi-drug resistance genes. Conclusions: ROR1 is expressed in HCC and contributes to disease development by interfering with multiple pathways. Acquired ROR1 expression may have diagnostic and prognostic value in HCC.
Pelin Balcik-Ercin, Metin Cetin, Irem Yalim-Camci, Gorkem Odabas, Nurettin Tokay, A. Emre Sayan, and Tamer Yagci
Springer Science and Business Media LLC