Lovastatin protects keratinocytes from DNA damage-related pro-apoptotic stress responses stimulated by anticancer therapeutics
详细信息 查看全文
- 作者：Verena Ziegler1 ; Anne Albers1 ; Gerhard Fritz ; fritz@uni-duesseldorf.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：53BP1 ; tumor suppressor p53 binding protein 1 ; ATM ; ataxia telangiectasia mutated ; ATR ; ataxia telangiectasia and Rad3-related ; Chk ; checkpoint kinase ; DSB ; DNA double-strand break ; DDR ; DNA damage response ; DNA-PKcs ; DNA-dependent protein kinase ; catalytic subunit ; Doxo ; doxorubicin ; 5-FU ; 5-fluorouracil ; γH2AX ; Ser139 phosphorylated histone H2AX ; HU ; hydroxyurea ; IR ; ionizing radiation ; JNK ; c-Jun N-terminal kinase ; Kap1 ; KRAB-associated protein 1 ; Lova ; HMG-CoA-reductase inhibitor lovastatin
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular Cell Research
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：1863
- 期：6
- 页码：1082-1092
- 全文大小：1995 K
文摘
- •
Lovastatin protects keratinocytes from IR- and Doxo-induced apoptosis.
- •
Doxorubicin-induced formation of DSBs is reduced by statin.
- •
Lovastatin reduces residual DNA damage following IR and Doxo treatment.
- •
Activation of ATR/Chk1 signaling by IR and Doxo is attenuated by statin.
- •
Protection by lovastatin involves proliferation-dependent and -independent mechanisms.