Renal cell carcinoma (RCC), following prostate and bladder tumours, is the third most prevalent genitourinary malignancy. Clear cell renal cell carcinoma makes up the bulk of RCC cases (ccRCC). Despite the fact that ccRCC is the most aggressive type of RCC, our understanding of its pathophysiology is limited. Previous research in our laboratory revealed important oncogenic roles of contactin 1 (CNTN1), a neuronal cell adhesion protein, in prostate cancer. CNTN1 is involved in a number of signalling pathways that are often changed in cancer, including the VEGFC-VEGF receptor 3 (VEFGR3)/fms-related tyrosine kinase 4 (Flt4) axis, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) axis, and the Notch signalling system. Collectively, evidence suggests that CNTN1 facilitates ccRCC. To examine this possibility, I have established stable ccRCC 786-O and A498 cell lines expressing either empty vector (EV) or CNTN1. In comparison to the respective EV lines, ectopic expression of CNTN1 enhances colony formation and cell proliferation. In comparison to A498 EV cells, A498 CNTN1 cells seems to possess enhanced migration ability based on wound healing assay. Taken together, my research provides in vitro evidence supporting CNTN1 in facilitating ccRCC pathogenesis. Future research will be required to investigate this concept using in vivo systems and primary ccRCC tumor tissues. / Thesis / Master of Science (MSc)