Exosomes are nano-sized membrane-bound secretory vesicles that are found in various biological fluids including blood. Exosomes play a significant role in regulating cell-to-cell communication both in normal physiological and especially in pathophysiological settings such as cancer. Hence, it is critical to study the pathways that are involved in the biogenesis and secretion of exosomes and their precise role in intercellular communication. In the current study, the role of oncogenic β‑catenin (CTNNB1) in the biogenesis and secretion of exosomes was investigated. It was observed that CRISPR/Cas9-based knockout of CTNNB1 attenuated Wnt signalling activity, reduced the proliferation as well as altered the morphology of HCT116 human colorectal cancer cells. In addition, the loss of oncogenic β-catenin upregulated cell cycle regulator protein p21, thereby inducing partial senescence. The induction of partial senescence in the CTNNB1-null HCT116 cells resulted in increased secretion of exosomes as evaluated by particle counting, protein quantification and Western blot analysis. Follow up analysis of immunofluorescence microscopy revealed upregulation of exosomal regulator proteins (Alix and CD63) in CTNNB1-null HCT116 cells, which resulted in the increased secretion of exosomes. Overall, this study revealed a novel role of oncogenic β‑catenin in regulating the secretion of exosomes from colorectal cancer cells.