Abstract
Basic transcription factor 3 (BTF3) is an RNA polymerase II transcription factor that also regulates apoptosis. Numerous studies have identified that BTF3 is aberrantly expressed in several types of tumor. However, the function of BTF3 in colorectal cancer remains unknown. The aim of the present study was to assess the function of BTF3 during colon cancer tumorigenesis. Applying a lentivirus-transfected short hairpin RNA approach, expression of BTF3 was dysregulated in the colon cancer HCT116 and HT-29 cell lines; knockdown efficiency was verified using the quantitative polymerase chain reaction and western blotting. To determine the function of BTF3 in colon cancer, cell proliferation was assessed using an MTT assay, cell apoptosis and the cell cycle were assessed using flow cytometry, and cell migration was assessed using a Transwell assay. Knockdown of BTF3 inhibited cell proliferation, possibly because BTF3 knockdown induced cell early apoptosis and arrested cells in G0-G1 phase. BTF3 knockdown also inhibited cell migration. The results of the present study identified that BTF3 expression is associated with colon cancer progress, and BTF3 may therefore be a molecular marker for diagnosis and treatment outcomes of human colon cancer.