@article {BODEAU1049, author = {SANDRA BODEAU and CHLO{\'E} SAUZAY and R{\'E}MY NYGA and CHRISTOPHE LOUANDRE and V{\'E}RONIQUE DESCAMPS and CATHERINE FRAN{\c C}OIS and CORINNE GODIN and GABRIEL CHOUKROUN and ANTOINE GALMICHE}, title = {Targeting the Unfolded Protein Response as a Potential Therapeutic Strategy in Renal Carcinoma Cells Exposed to Cyclosporine A}, volume = {37}, number = {3}, pages = {1049--1057}, year = {2017}, publisher = {International Institute of Anticancer Research}, abstract = {Background/Aim: Organ transplant patients treated with the immunosuppressive drug cyclosporine A often present malignant kidney tumors. Cyclosporine A can promote oncogenesis in a cell-intrinsic manner by increasing the production of vascular endothelial growth factor (VEGF). Materials and Methods: We explored the impact of cyclosporine A and the role of the unfolded protein response (UPR) on three human renal cell carcinoma (RCC) cell lines under normoxic and hypoxic (1\% O2) conditions. Results: Cyclosporine A regulated the expression of VEGF at the post-transcriptional level. Cyclosporine A induced the inositol requiring enzyme-1α (IRE1α) arm of the UPR and stabilized neosynthesized proteins in RCC cells. Toyocamycin, an inhibitor of IRE1α, abolished the clonogenic growth of RCC cells and reduced induction of VEGF by cyclosporine A under hypoxia. Conclusion: Our findings highlight the impact of cyclosporine A on the proteostasis of RCC cells, and suggest the potential therapeutic interest of targeting the UPR against tumors arising in the context of organ transplantation.}, issn = {0250-7005}, URL = {https://ar.iiarjournals.org/content/37/3/1049}, eprint = {https://ar.iiarjournals.org/content/37/3/1049.full.pdf}, journal = {Anticancer Research} }