C/EBPβ regulates the JAK/STAT signaling pathway in triple-negative breast cancer

被引：10
|
作者：
Wang, Shu [1 ]
Xia, Dian [1 ]
Wang, Xianzhi [1 ,2 ]
Cao, Haowei [1 ]
Wu, Chaoshen [1 ]
Sun, Zhaoran [1 ]
Zhang, Daoyong [1 ]
Liu, Hao [2 ]
机构：
[1] Xuzhou Med Univ, Jiangsu Key Lab Brain Dis & Bioinformat, Xuzhou, Jiangsu, Peoples R China
[2] Bengbu Med Coll, Sch Pharm, Bengbu, Peoples R China
来源：
FEBS OPEN BIO | 2021年 / 11卷 / 04期
基金：
中国国家自然科学基金;
关键词：
C/EBP beta; JAK; STAT; Triple-Negative Breast Cancer;
D O I：
10.1002/2211-5463.13138
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：
C/EBP beta is a member of the CCAAT/enhancer-binding protein (C/EBP) family, which consists of a number of b-ZIP transcription factors. Although C/EBP beta has been implicated in the development of certain cancers, including breast cancer, it remains unknown whether dysregulation of C/EBP beta in breast cancer is subtype-specific. Moreover, the underlying mechanisms by which C/EBP beta regulates breast cancer carcinogenesis are not fully understood. Here, we present evidence that C/EBP beta is specifically overexpressed in human TNBC samples, but not in non-TNBC samples. C/EBP beta depletion dramatically suppressed TNBC cell growth, migration, invasion, and colony formation ability. A subsequent mechanistic study revealed that the JAK/STAT signaling pathway was upregulated in C/EBP beta_high TNBC samples compared with C/EBP beta_low TNBC samples. C/EBP beta ChIP-seq and qPCR were performed to demonstrate that C/EBP beta directly binds to and regulates JAK/STAT signaling pathway genes in TNBC. Taken together, our data indicate the oncogenic role of C/EBP beta in human TNBC and reveal a novel mechanism by which C/EBP beta promotes TNBC carcinogenesis.
引用
收藏
页码：1250 / 1258
页数：9
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