Colorectal cancer (CRC) arises as a result of accumulated mutations in key proteins that regulate cell proliferation, differentiation and death. Large scale sequencing studies have established the predominance of mutations in proteins involved in Wnt signaling pathway in a large number of CRC patients. It was also shown that over 90% of sporadic CRC cases, harboured mutation in APC and/or β-catenin gene involved in Wnt signaling pathway. Recently, Wnt ligands have shown to play an important role in facilitating Wnt signaling pathway invivo. However, the process of Wnt trafficking between cells remains elusive. As Wnt proteins are insoluble due to their hydrophobic nature, carrier mechanisms that facilitate their export from endoplasmic reticulum to the cell surface are required. One of the proposed mechanisms of intercellular signaling involves extracellular vesicles (EVs) which act as messengers carrying oncogenes from malignant to non-malignant target cells. Extracellular vesicles (EVs) are diverse in nature and are released by a variety of cells including normal and cancerous cells during physiological and pathological conditions. These EVs carrying Wnt signaling components can ultimately lead to Wnt-driven cancers in the surrounding cells. We hypothesised that a) EVs derived from LIM1215 CRC cells carrying mutated β-catenin could activate Wnt signaling pathway in recipient cells. b) EVs derived from LIM1215 cells could also exert proliferative effects on recipient cells. In order to rule out the fact that other Wnt components in EVs are responsible for Wnt signaling activity, a β-catenin knockout LIM1215 cells were generated. Additionally, SILAC approach was followed to confirm the transfer of mutant β-catenin to the nucleus of the recipient cells leading to activation of Wnt signaling. In the second part of the project, the role of EVs derived from LIM1215 cells were examined on cells commonly found in tumour microenvironment (TM). We hypothesised that EVs mediate signaling pathway in recipient cells by transfer of phospho-proteins. To achieve this, EVs were incubated with the recipient cells and quantitative proteomics (including whole and phospho-proteomics) coupled with di-methyl labelling was performed. In addition, quantitative proteomics was complemented by targeted antibody based analysis.