Prof. Gulberk Ucar
Hacettepe University, Turkiye
Prof. Dr. GULBERK UCAR
She graduated from Hornell Senior High School (USA) in 1975, and from the Faculty of Pharmacy, Hacettepe University (HU) in 1979. Between 1981 and 1991, she worked as a research assistant at Hacettepe University, Faculty of Pharmacy, Department of Biochemistry. She received her master's and doctoral degrees from Hacettepe University Institute of Health Sciences Medical Biochemistry Program in 1983 and 1991. She received the title of assistant professor in 1992, associate professor in 1996, and professor in 2005 in the Biochemistry Department of the Faculty of Pharmacy, Hacettepe University. She served as the Head of the same Department between 2005-2020 and simultaneously as the Head of the Department of Basic Pharmaceutical Sciences between 2017-2020.
She conducted her scientific research in L’Istitut Pasteur, Paris (France), La Faculté de Médecine de Strasbourg (France), Karolinska Instutet (İsveç), Universitat Autònoma de Barcelona (Spain), Max-Planc Institut für Biochemie, München (Germany), and The Morsani College of Medicine, USF, Tempa (USA). She held many scientific and administrative positions such as executive memberhip/chairmanship/presidency/ coordinatorship in the Executive committees and Institutions of Hacettepe University as well as in several national and international scientific associations and committees. She served as editor/co-editor or executive member in Advisory/Editorial Boards of many national or international scientific publications. She is currently the Dean of the Faculty of Pharmacy, Hacettepe University, and the President of “The society of Researchers in Pharmacy and Medicine, ILARUD. She has 8 national and 2 international awards, She has over 200 national/international scientific publications with a high rate of citations; over 250 national/international oral/poster presentations, and also several national/ international scientific projects. Her h index is 35. She speaks English, French, and German. She is married and has one child.
Targetting Epithelial-Mesenchymal Transition (EMT) in Cancer Treatment
Gulberk UÇAR1, Burçin ÖZÇELİK2, Seyhan TURK1, İpek BAYSAL3, Açelya ERİKÇİ4, Bercis İmge Uçar GÖKER5, Alper Bektaş İSKİT6.
1 Department of Biochemistry, Faculty of Pharmacy, Hacettepe University, Ankara, Türkiye
2Department of Molecular Biology and Geenetics, Faculty of Arts and Sciences, Hitit University, Corum, Türkiye
3Department of Pharmacy Services, Vocational School of Health Services, Hacettepe University, Ankara, Türkiye
4Department of Biochemistry, Faculty of Pharmacy, Lokman Hekim University, Ankara, Türkiye
5Department of General Surgery, Faculty of Medicine, Kutahya Health Sciences University, Kutahya, Türkiye
6Department of Medical Pharmacology, Faculty of Medicine, Hacettepe University, Ankara, Türkiye
Cancer, a leading global health concern, is characterized by uncontrolled cell proliferation, resulting in a myriad of complications. The identification of specific molecular markers associated with various cancer types has paved the way for targeted therapies and personalized medicine. Among these markers, the epithelial-mesenchymal transition (EMT) has garnered significant attention due to its pivotal role in cancer metastatic spread and treatment resistance.
EMT is a complex process involving a cascade of molecular events wherein epithelial cells undergo a transformation. Since EMT involves a comprehensive reprogramming of epithelial cells, leading to a loss of their characteristic cellular adhesion and polarity, while simultaneously acquiring mesenchymal traits, it is intricately linked to invagination, migration, plasticity, and malignancy. EMT is instrumental in the malignant progression of neoplasms, contributing significantly to the increased metastatic potential and therapy resistance in cancer cells. Interaction among cancer cells in the tumor microenvironment has been shown to induce EMT by auto- and ⁄ or paracrine secretion of mediators such as growth factors, cytokines, and ECM proteins.The understanding EMT will enable elucidation of the complex molecular and cellular dynamics underlying tumor progression and will also pave the way for new and more effective therapeutic approaches. Recently, addressing EMT represents a significant challenge in the development of advanced cancer therapeutics.
Colorectal cancer (CRC) is the second-leading cause of cancer-related death in the World. EMT has become a hot issue in CRC because strong inducers of EMT (such as TGF-β) can initiate EMT and regulate metastasis, microenvironment, and immune system resistance in CRC. Despite advances in cytotoxic and targeted therapy, resistance to chemotherapy remains as one of the greatest challenges in long-term management of incurable metastatic CRC. Although EMT has been found to play a critical role in CRC drug resistance and metastasis, the nature of the intrinsic links remains unclear. Current strategies for targeting EMT is to inhibit the EMT to prevent metastasis and invasionand to reverse the EMT to restore the epithelial characteristics of cancer cells, making them more sensitive to treatment.
Present study delves into the multifaceted factors that influence EMT regulation in cancer progression, metastasis and drug resistance, and summarizes the studies conducted by our cancer research group on targeting of EMT in cancer, especially colorectal cancer.
