Oil-in-water (‘inverse’) High Internal Phase Emulsions (HIPEs) have been prepared using an amphiphilic macro-RAFT agent with toluene as the internal dispersed phase (∼80 vol%) and an aqueous monomer solution as the continuous phase. The water phase consisted of the monomers acrylamide (AM) and N,N′-methylenebisacrylamide (MBAM), an initiator as well as the amphiphilic macro-RAFT agent, that is 2-(butylthiocarbonothioylthio)-2-poly(n-butyl acrylate)-b-poly(acrylic acid), which was used as an anionic polymeric surfactant. The presence of these amphiphilic species allowed the successful preparation of a polyHIPE upon polymerization. The effect of concentration of macro-RAFT agent, pH, initiator, hexadecane as an organic modifier and the polymerization temperature on the morphology of the resulting porous materials was investigated. Varying the lengths of the hydrophilic and hydrophobic blocks of the macro-RAFT agent resulted in polyHIPEs with different porous structures. The presence of RAFT functionality in the polyHIPE was confirmed by elemental analysis, EDX-SEM, Raman and FT-IR spectroscopies. Raman mapping revealed full coverage of the void walls with dithiocarbamate groups.

Chemoresistance remains the major barrier to effective ovarian cancer treatment. The molecular features and associated biological functions of this phenotype remain poorly understood. We developed carboplatin-resistant cell line models using OVCAR5 and CaOV3 cell lines with the aim of identifying chemoresistance-specific molecular features. Chemotaxis and CAM invasion assays revealed enhanced migratory and invasive potential in OVCAR5-resistant, compared to parental cell lines. Mass spectrometry analysis was used to analyse the metabolome and proteome of these cell lines, and was able to separate these populations based on their molecular features. It revealed signalling and metabolic perturbations in the chemoresistant cell lines. A comparison with the proteome of patient-derived primary ovarian cancer cells grown in culture showed a shared dysregulation of cytokine and type 1 interferon signalling, potentially revealing a common molecular feature of chemoresistance. A comprehensive analysis of a larger patient cohort, including advanced in vitro and in vivo models, promises to assist with better understanding the molecular mechanisms of chemoresistance and the associated enhancement of migration and invasion.