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• W2132110907 abstract "Current cancer treatments are associated with high mortality because anticancer drugs are highly toxic and have numerous side effects. Human α-lactalbumin Made Lethal to Tumour cells (HAMLET) is protein-lipid complex that kills tumor cells and spares healthy differentiated cells. HAMLET interacts with a broad range of cellular targets. Our group has shown that the cell death induced by HAMLET can be correlated with a caspase independent pathway, a transcriptional response characterized by the activation of ion fluxes and p38 MAPK signalling pathway. There are still many cellular events in response to HAMLET that need to be address. HAMLET is isolated from a casein fraction of human milk and Casein Kinase 1 (CK1) has been shown to phosphorylate several proteins contained in casein. Furthermore CK1 has been showed to phosphorylate the partially unfolded state of α-lactalbumin compared to its native state. For this reason we wanted to investigate if there was any functional interaction between HAMLET and CK1. Here we showed by a protoarray, confocal imaging, and co-IP assays that HAMLET interacts with CK1 isoforms. Treatment of cancer cells with HAMLET triggered a marked change in distribution of CK1 isoforms. CK1δ was found to accumulate in a network of filaments corresponding to the cytoskeleton, as confirmed by CK1δ colocalization with α-actinin1. This was explained by HAMLET inhibition of CK1δ dependent phosphorylation of Tau. CK1α and CK1e accumulated in the perinuclear region of the cell. The perinuclear compartment was identified as the endoplasmic reticulum (ER) as confirmed by CK1α colocalization with the ER marker, calnexin. HAMLET triggered a marked ER stress response by activation of all the three main branches of the Unfolded Protein Response (UPR): activation of the inositol requiring protein 1 (IRE1), the protein kinase RNA-like endoplasmic reticulum kinase (PERK) and the activating transcription factor 6 (ATF6). Involvement of CK1 in the ER stress response triggered by HAMLET still needs to be clarified. Furthermore, inhibition of CK1 isoforms with the CK1 specific inhibitor IC261 caused partial inhibition in HAMLET induced CK1 distribution and caused synergistic cell death. Finally, ion fluxes which are essential for HAMLET-induced tumor cell death partially prevented CK1 change in distribution. (Less)" @default.
• W2132110907 created "2016-06-24" @default.
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• W2132110907 date "2015-01-01" @default.
• W2132110907 modified "2023-09-26" @default.
• W2132110907 title "Functional Interaction between Casein Kinase 1 and HAMLET" @default.
• W2132110907 hasPublicationYear "2015" @default.
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