Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of replicative senescence

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• 作者：Antonella Marino Gammazza^a ; ^b ; ^{antonella.marino@hotmail.it} ; Claudia Campanella^a ; ^b ; Rosario Barone^a ; ^b ; Celeste Caruso Bavisotto^a ; ^b ; Magdalena Gorska^c ; Michal Wozniak^c ; Francesco Carini^a ; Francesco Cappello^a ; ^b ; Antonella D'Anneo^d ; Marianna Lauricella^e ; Giovanni Zummo^a ; Everly Conway de Macario^f ; ^g ; Alberto J.L. Macario^b ; ^f ; ^g ; Valentina Di Felice^a ; ^b
• 关键词：Doxorubicin ; Hsp60 ; Acetylation ; Ubiquitination ; p53 ; Replicative senescence
• 刊名：Cancer Letters
• 出版年：2017
• 出版时间：28 January 2017
• 年：2017
• 卷：385
• 期：Complete
• 页码：75-86
• 全文大小：2485 K
• 卷排序：385

文摘

Low doxorubicin doses induce replicative senescence in human lung mucoepidermoid carcinoma cells. Cells treated with doxorubicin show a reduction of Hsp60 levels and an increase in its acetylation. Hsp60 acetylation may induce the destabilization of the pro-tumor Hsp60/p53 complex in these cells. p53 may exert its tumor suppressive function by activating p53-dependent cell senescence pathway via the induction of p21.