Prostate cancer (PCa) is dependent on androgens for growth. Androgen deprivation therapy (ADT) curtails PCa progression, however this powerful selective pressure leads to aggressive, castrate resistant PCa. One castrate resistant prostate cancer subtype, neuroendocrine (NE) PCa, is characterised by increased abundance of NE cells. Transdifferentiation into androgen independent NE-like cells is thought to allow PCa epithelial cells to escape potent ADT, causing resistance. NE-like cells are thought to promote growth of surrounding tumour cells through paracrine communication. Exosomes are small extracellular vesicles released from all cells. They can be endocytosed by neighbouring cells and modify cellular function through their cargo (proteins and RNAs). Exosomes have been proposed to promote PCa NE-transdifferentiation (NEtD); by an unknown mechanism. This project aimed to isolate and characterise exosomes from NE-like cells and investigate their potential role in driving neuroendocrine PCa. LNCaP cells were cultured in media containing charcoal-stripped FCS to deplete androgens as an in vitro model of AD (androgen deprivation) to promote NEtD. NEtD was confirmed by analysing LNCaP morphology, immunoblotting and qRT PCR, investigating markers of the androgen receptor and NEtD. Exosomes are prevalent in FCS and may mask exosomes released from NE-like LNCaP cells, therefore exosomes were depleted from FCS/charcoal-stripped FCS by differential centrifugation. Exosome depletion did not affect LNCaP NEtD morphology or expression of androgen receptor and NEtD markers. However, AD increased expression of markers of the exosomal machinery (ALIX, CD9, HSP70 TSG101, RAB27A, VAMP7) as seen by qRT-PCR, suggesting AD may enhance exosome production. Exosomes were isolated from LNCaP and NE-like LNCaP culture medium to analyse exosome size, number and content by dynamic light scattering and immunoblotting. AD increased exosomal number and CD9 expression, suggesting NEtD is associated with increased exosome release. Exosome release from LNCaP cells was reduced by GW4869 and enhanced by Monensin. GW4869 regressed NEtD in AD LNCaP cells while Monensin induced NEtD in control LNCaP cells and enhanced AD LNCaP cells.