Investigation of the role in some cancer stem cells on cancer formation in melanoma cell line (B16F10) and the effects of antiparasitic agents on cancer formation through hedgehog signaling pathway

Melanoma is a malignant tumor that arises from neural clefts and occurs as a result of transformation of melanocytes that produce melanin pigment. 90%of cancer-related deaths occur in metastatic cancer conditions and melanoma is one of the deadliest cancers known. In general, melanoma accounts for 1-3% of all malignant tumors and its incidence increases by 6-7% each year. Frequent resistance to conventional treatments in patients with melanoma; melanoma-specific CSCs and the regulatory mechanisms of CSCs necessitate the development of new effective and selective therapeutic chemicals that specifically target signaling pathways. In our study, in order to identify and develop potentially more effective treatment methods, skin cancer was created in mouse by sorting cells with surface markers CD133+ and CD133- from the melanoma cancer cell line (B16F10) in order to reveal and identify new compounds that have the ability to eliminate cancer and cancer stem cells. As a result of our studies, we observed that Ornidazole inhibited mouse melanoma B16 cell proliferation and migration as a dose and time depended manner in vitro compared to control groups in our experimental groups treated with Ornidazole. We also observed that Ornidazole treatment aggravated DNA damage. Moreover, with mouse melanoma model tumor analysis, we observed that Ornidazole reduced the melanoma volume. Taken together, our findings showed that Ornidazole reduced melanoma progression and simultaneously suppressed Hedhegog signaling pathway and autophagy expression and induced apoptosis. In addition, Ornidozole was found to induce ER stress-mediated apoptosis expression and inhibit ER stress-mediated autophagy expression. Our findings show that Ornidazole may play a role in tumor growth inhibition. Keywords: Melanoma, Cancer Stem Cell, Ornidazole, CD133, Hedgehog signaling pathway, ER stress.