当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > BTF3 promotes stemness and inhibits TypeⅠInterferon signaling pathway in triple-negative breast cancer.

BTF3 promotes stemness and inhibits TypeⅠInterferon signaling pathway in triple-negative breast cancer.

Abstract：

:Triple-negative breast cancer (TNBC) is a major challenge in clinical practice due to its aggressiveness and lack of targeted treatment. Cancer stem-like traits contribute to tumorigenesis and immune privilege of TNBC. However, the relationship of stemness and immunosurveillance remains unclear. Here, we demonstrate that BTF3 expression is related with stem-like properties in TNBC cells. BTF3 modulates stemness, migration and proliferation of TNBC in vitro. Bioinformatics analysis revealed that interferon signaling pathways and IRF7, both of which participate in the immune escape of TNBC, are closely related to BTF3 in TNBC cells. Knockdown of BTF3 activates IRF7 expression through increased degradation of BMI1, a protein that can represses IRF7 transcription by directly binding to its promotor region. BTF3 links stem-like traits and the interferon signaling pathway, revealing the potential connection of stemness and immunomodulation in TNBC. Clinically, we suggest that BTF3 is predictive of poor prognosis in patients with TNBC. Together, our findings highlight an important role of BTF3 in regulating the progression of TNBC cells.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang H,Gao L,Qi M,Su P,Xiong X,Zhao J,Hu J,Han B

doi

10.1016/j.bbrc.2020.12.060

subject

Has Abstract

pub_date

2021-01-22 00:00:00

pages

22-28

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)32237-3

journal_volume

537

pub_type

杂志文章

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