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

页码：314 / 320

页数：7

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