Marino Gammazza, Antonella <br/><br/>
Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of replicative senescence.  [electronic resource] 

 -  Cancer letters  01 2017 
 - 75-86 p.  digital 
<br/><br/> Publication Type: Journal Article 
<br/><br/><label>ISSN: </label>1872-7980 
<br/><br/><label>Standard No.: </label>10.1016/j.canlet.2016.10.045  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Acetylation<br/>Antibiotics, Antineoplastic--pharmacology<br/>Apoptosis--drug effects<br/>Carcinoma, Mucoepidermoid--drug therapy<br/>Cell Line, Tumor<br/>Cell Proliferation--drug effects<br/>Cell Survival--drug effects<br/>Cellular Senescence--drug effects<br/>Chaperonin 60--genetics<br/>Chaperonins--metabolism<br/>Cyclin-Dependent Kinase Inhibitor p21--metabolism<br/>Dose-Response Relationship, Drug<br/>Doxorubicin--pharmacology<br/>G2 Phase Cell Cycle Checkpoints--drug effects<br/>Histones--metabolism<br/>Humans<br/>Lung Neoplasms--drug therapy<br/>Mitochondrial Proteins--genetics<br/>Protein Binding<br/>Protein Processing, Post-Translational--drug effects<br/>Proteolysis<br/>Signal Transduction--drug effects<br/>Tumor Suppressor Protein p53--metabolism<br/>Ubiquitination