PO-112 The role of transcribed ultraconserved regions Uc160 and Uc346 in colorectal cancer progression

Introduction Expression of Transcribed Ultra Conserved Regions (Transcribed Ultra Conserved Regions, T-UCRs) is often deregulated in many types of cancer, including colorectal cancer (CRC). Our previous results showed that T-UCRs Uc160 and Uc346 are methylated in CRC. Additionally, their tumour methylation is associated with time to disease progression (TTP) and appears to be a promising biomarker for CRC. However, their role in CRC progression has not been elucidated to date. Material and methods Aim of the study was to investigate the role of Uc160 and Uc346 in proliferation, motility and migration in colon cancer cells. For that purpose, Uc160 and Uc346 were cloned into plasmids and three colon cancer cell lines (HT-29, Caco-2 and DLD-1) were transiently transfected. After overexpression of Uc160 and Uc346, proliferation (MTT assay), motility (scratch wound healing assay) and migration (transwell migration assay) rates were evaluated. Results and discussions Proliferation rates, 48 hour after overexpression, were higher in the transfected cells in all cell lines, compared with the control cells (mock transfected). The most significant differences in proliferation rates were noticed for Uc160 overexpression in Caco-2 (p=0.008) and Uc346 overexpression in DLD-1 cells (p=0.033). Similar results were observed in motility assay, with cells overexpressing Uc160 or Uc346 having higher motility rates compared to control cells in all cell lines. More specifically, most significant differences in motility rates were observed in HT-29 and DLD-1 cells overexpressing Uc160 or Uc346 (p=0.017, p=0.041 and p=0.023, p=0.004 respectively). Further analysis of DLD-1 cells migration confirmed the above results, with higher number of Uc160 or Uc346 overexpressing cells migrating compared to the control cells (p=0.005 for both T-UCRs). Conclusion T-UCRs Uc160 and Uc346 appear to affect the proliferation, motility and migration rates of colon cancer cells, implicating a complex role in CRC progression.