Resistance to paclitxel in breast carcinoma cells requires a quality control of mitochondrial antiapoptotic proteins by TRAP1

• Published in: Molecular oncology Vol. 7; no. 5; pp. 895 - 906
• Main Authors: Maddalena, Francesca, Sisinni, Lorenza, Lettini, Giacomo, Condelli, Valentina, Matassa, Danilo Swann, Piscazzi, Annamaria, Amoroso, Maria Rosaria, La Torre, Giuseppe, Esposito, Franca, Landriscina, Matteo
• Format: Journal Article
• Language: English
• Published: United States Elsevier B.V 01.10.2013; John Wiley & Sons, Inc; John Wiley and Sons Inc
• Subjects: Adaptation; Antineoplastic Agents, Phytogenic - pharmacology; Apoptosis; Apoptosis - drug effects; Apoptosis Regulatory Proteins - genetics; Apoptosis Regulatory Proteins - metabolism; Breast cancer; Breast carcinoma; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Cancer therapies; Cell culture; Clonal deletion; Cytotoxicity; Deletion mutant; Drug resistance; Endoplasmic reticulum; Endoplasmic Reticulum Stress - drug effects; ER stress; Female; Homeostasis; HSP90 Heat-Shock Proteins - genetics; HSP90 Heat-Shock Proteins - metabolism; Hsp90 protein; Humans; Hypotheses; Immunoblotting; Localization; Mitochondria; Mitochondrial Proteins - genetics; Mitochondrial Proteins - metabolism; Paclitaxel; Paclitaxel - pharmacology; Prostate; Proteins; Quality control; Reverse Transcriptase Polymerase Chain Reaction; siRNA; Stress response; Transfection; TRAP1; Tumor cells; Tumors; United States > US; ER stress; TRAP1; Breast carcinoma; Drug resistance; Paclitaxel; Apoptosis

TRAP1 is a mitochondrial antiapoptotic protein up-regulated in several human malignancies. However, recent evidences suggest that TRAP1 is also localized in the endoplasmic reticulum (ER) where it is involved in ER stress protection and protein quality control of tumor cells. Based on the mechanisti...