Investigation of the apoptotic and antiangiogenic effects of boron in human colon cancer (CCL-233) cells

INVESTIGATION OF THE APOPTOTIC AND ANTIANGIOGENIC EFFECTS OF BORON IN CCL-233 CELLS IN HUMAN COLON CANCER (M. Sc. Thesis) Şahabettin Can ÖZYARIM UNIVERSITY OF UŞAK GRADUATE EDUCATION INSTITUTE June 2020 ABSTRACT Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide, and remains one of the leading causes of cancer-related death. Recent research has shown that microbial and environmental factors, including diet and lifestyle, may affect the development of colon cancer. The success rates of the methods used for colorectal cancer treatment are very low. Boron is an important mineral that plays an important role in various biological processes. Boron is necessary for the growth of plants, animals and humans. Borik asit ve boraks, bor denilen bu bileşiklerin en önemlileridir. Borik asidin bazı önemli kimyasal özellikleri, kanser tedavisinde kullanımını desteklemektedir. Studies have demonstrated that bone density, embryonic development, wound healing and cancer treatment are associated with other benefits of boron in animals and humans fed the boron diet. Boron has also been reported to affect the metabolism of various enzymes and minerals. In this thesis, the effects of boric acid on CCl-233 human colon adenocarcinoma cell lines were investigated by proliferation, VEGF and PARP analysis studies. As a result of the studies; cell viability analysis showed that 50 mM boric acid decreased cell proliferation after 24, 48 and 72 hours. The best results were found at 48 hours. At 48 hours performed PARP analysis was then. PARP values were higher in cisplatin applied iv control group. In contrast, PARP levels were low at two levels of boron (50-100 mM). In addition to this analysis, VEGF analysis was performed at 48th hour and it was observed that VEGF boron levels differed with cisplatin and there was no difference between control groups. Keywords : Colon Cancer, Boric acid, Proliferation, VEGF, PARP