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C/EBPβ regulates the JAK/STAT signaling pathway in triple‐negative breast cancer
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016132/ https://www.ncbi.nlm.nih.gov/pubmed/33660927 http://dx.doi.org/10.1002/2211-5463.13138 |
Sumario: | 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. |
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