Open AccessC/EBPβ regulates the JAK/STAT signaling pathway in triple‐negative breast cancer
Author(s) -
Wang Shu,
Xia Dian,
Wang Xianzhi,
Cao Haowei,
Wu Chaoshen,
Sun Zhaoran,
Zhang Daoyong,
Liu Hao
Publication year - 2021
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.13138
Subject(s) - triple negative breast cancer , cancer research , carcinogenesis , ccaat enhancer binding proteins , stat , signal transduction , transcription factor , biology , breast cancer , cell growth , cancer , gene , stat3 , microbiology and biotechnology , dna binding protein , genetics
C/EBPβ is a member of the CCAAT/enhancer‐binding protein (C/EBP) family, which consists of a number of b‐ZIP transcription factors. Although C/EBPβ has been implicated in the development of certain cancers, including breast cancer, it remains unknown whether dysregulation of C/EBPβ in breast cancer is subtype‐specific. Moreover, the underlying mechanisms by which C/EBPβ regulates breast cancer carcinogenesis are not fully understood. Here, we present evidence that C/EBPβ is specifically overexpressed in human TNBC samples, but not in non‐TNBC samples. C/EBPβ 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/EBPβ_high TNBC samples compared with C/EBPβ_low TNBC samples. C/EBPβ ChIP‐seq and qPCR were performed to demonstrate that C/EBPβ directly binds to and regulates JAK/STAT signaling pathway genes in TNBC. Taken together, our data indicate the oncogenic role of C/EBPβ in human TNBC and reveal a novel mechanism by which C/EBPβ promotes TNBC carcinogenesis.