STAT3 inhibition as a therapeutic strategy for leukemia

被引：17

作者：

Kanna, Rubashruti ^{[1
]}

Choudhary, Gaurav ^{[1
]}

Ramachandra, Nandini ^{[1
]}

Steidl, Ulrich ^{[1
]}

Verma, Amit ^{[1
]}

Shastri, Aditi ^{[1
]}

机构：

[1] Albert Einstein Coll Med, Dept Oncol, Div Hematol Malignancies, 1300 Morris Pk Avenuem, Bronx, NY 10461 USA

来源：

LEUKEMIA & LYMPHOMA | 2018年 / 59卷 / 09期

关键词：

Leukemia; signal transduction; transcription factor changes; MYELOID-LEUKEMIA; CELLS; CANCER; ACTIVATION; APOPTOSIS; STEM;

D O I：

10.1080/10428194.2017.1397668

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Leukemia is characterized by selective overgrowth of malignant hematopoietic stem cells (HSC's) that interfere with HSC differentiation. Cytoreductive chemotherapy can kill rapidly dividing cancerous cells but cannot eradicate the malignant HSC pool leading to relapses. Leukemic stem cells have several dysregulated pathways and the Janus kinases (JAKs) and signal transducer and activator of transcription (STAT) pathway are prominent among them. STAT3 is an important transcription factor that regulates cell growth, proliferation, and inhibits apoptosis. High STAT3 expression in leukemia has been associated with an increased risk for relapse and decreased overall survival. Multiple strategies for interfering with STAT3 activity in leukemic cells include inhibition of STAT3 phosphorylation, interfering with STAT3 interactions, preventing nuclear transfer, inhibiting transcription and causing interference in STAT: DNA binding. A better understanding of key interactions and upstream mediators of STAT3 activity will help facilitate the development of effective cancer therapies and may result in durable remissions.

引用

页码：2068 / 2074

页数：7

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