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Identification of FOXE3 transcription factor as a potent oncogenic factor in triple-negative breast cancer.

Abstract：

:Triple-negative breast cancer (TNBC) represents a unique subgroup of breast cancers (BCa) with potential to be highly proliferative and invasive. Patient with TNBC are prone to developing resistance to chemotherapy. Therefore, TNBC usually has a poor clinical outcome. The key factors driving these malignant features remain poorly understood. In this study, we report for the first time that expression levels of FOXE3, a recently identified lens-specific transcription factor, were preferentially upregulated in TNBC tissues compared to non-TNBC tissues, and this upregulation correlated well to a poor overall/recurrence-free survival in patients. Depletion of FOXE3 in TNBC cell lines promoted cell death, cell cycle arrest, and potentiated sensitivity to docetaxel (DTX), a first-line chemotherapeutic drug for TNBC treatment. These alterations in cell growth/survival properties were accompanied by induction of CDKN1B, a gene encoding the tumor suppressor p27. We further provided the molecular evidence that FOXE3 could directly bind to the CDKN1B promoter and negatively regulate its transcription in TNBC cells. Importantly, knockdown of combined p27 and FOXE3 reversed the DTX-induced cell growth inhibition observed upon FOXE3 knockdown, indicating that the FOXE3's effects on TNBC progression were mediated mainly through transcriptional regulation of the p27 signaling. Together, our findings suggest that FOXE3 may function as a potent oncogene during the progression of TNBC, likely affecting cell proliferation, invasion and chemosensitivity, and functioning at least in part through transcriptional repression of p27 signaling.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wang H,Yang T,Yuan Y,Sun X

doi

10.1016/j.bbrc.2019.12.034

subject

Has Abstract

pub_date

2020-02-26 00:00:00

pages

78-85

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(19)32354-X

journal_volume

523

pub_type

杂志文章

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