Fludarabine nucleoside induces major changes in the p53 interactome in human B-lymphoid cancer cell lines

被引：0
|
作者：
Almazi, Juhura G. [1 ,2 ]
Alomari, Munther [1 ,3 ]
Belov, Larissa [1 ]
Best, O. Giles [4 ]
Shen, Yandong [1 ]
Graham, Mark E. [5 ]
Mulligan, Stephen P. [1 ,4 ]
Christopherson, Richard I. [1 ]
机构：
[1] Univ Sydney, Sch Life & Environm Sci, Sydney, NSW 2006, Australia
[2] Univ Sydney, Woolcock Inst Med Res, Resp Technol, Sydney, NSW, Australia
[3] Imam Abdulrahman Bin Faisal Univ, Dept Stem Cell Biol, Inst Res & Med Consultat, Dammam, Saudi Arabia
[4] Royal North Shore Hosp, Kolling Inst Med Res, Hematol, St Leonards, NSW, Australia
[5] Univ Sydney, Childrens Med Res Inst, Westmead, NSW, Australia
来源：
NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS | 2022年 / 41卷 / 03期
关键词：
Fludarabine; leukemia; p53; drug mechanism; interactome; HUMAN RAJI;
D O I：
10.1080/15257770.2021.2013500
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Triple combination FCR (fludarabine, cyclophosphamide and rituximab) is often used as front-line treatment for chronic lymphocytic leukemia (CLL) and non-Hodgkin's lymphoma. Results from our laboratory indicate that 2-FaraAMP (fludarabine) has multiple mechanisms of cytotoxicity that include accumulation of isoforms and phosphorylated derivatives of p53, and induction of the unfolded protein response (UPR). Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells. These changes are likely driven by DNA strand breaks induced by 2-FaraA that activate protein kinases such as ATM, ATR and Chk1.
引用
收藏
页码：314 / 320
页数：7
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