E2F3 drives the epithelial-to-mesenchymal transition, cell invasion, and metastasis in breast cancer.
Animals
Carcinogenesis
/ genetics
Cell Line, Tumor
Cell Movement
/ genetics
Cell Proliferation
/ genetics
E2F3 Transcription Factor
/ genetics
Epithelial-Mesenchymal Transition
/ genetics
Female
Gene Expression Regulation, Neoplastic
/ genetics
Male
Mice
Mice, SCID
Signal Transduction
/ genetics
Triple Negative Breast Neoplasms
/ genetics
E2F3
Shugoshin-1
epithelial-to-mesenchymal transition
invasion
triple-negative breast cancer
Journal
Experimental biology and medicine (Maywood, N.J.)
ISSN: 1535-3699
Titre abrégé: Exp Biol Med (Maywood)
Pays: England
ID NLM: 100973463
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
pubmed:
10
8
2021
medline:
15
12
2021
entrez:
9
8
2021
Statut:
ppublish
Résumé
E2F3 is a transcription factor that may initiate tumorigenesis if overexpressed. Previously, we demonstrated that E2F3 mRNA is overexpressed in breast cancer and that E2F3 overexpression results in centrosome amplification and unregulated mitosis, which can promote aneuploidy and chromosome instability to initiate and sustain tumors. Further, we demonstrated that E2F3 leads to overexpression of the mitotic regulator Shugoshin-1, which until recently had unknown roles in cancer. This study aims to evaluate the roles of E2F3 and Shugoshin-1 in breast cancer metastatic potential. Here we demonstrated that E2F3 and Shugoshin-1 silencing leads to reduced cell invasion and migration in two mesenchymal triple-negative breast cancer (TNBC) cell lines (MDA-MB-231 and Hs578t). Moreover, E2F3 and Shugoshin-1 modulate the expression of epithelial-to-mesenchymal transition-associated genes such as Snail, E-Cadherin, and multiple matrix metalloproteinases. Furthermore, E2F3 depletion leads to reductions in tumor growth and metastasis in NOD-
Identifiants
pubmed: 34365840
doi: 10.1177/15353702211035693
pmc: PMC8524769
doi:
Substances chimiques
E2F3 Transcription Factor
0
E2F3 protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2057-2071Subventions
Organisme : NIGMS NIH HHS
ID : R25 GM082406
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007579
Pays : United States
Organisme : NIGMS NIH HHS
ID : U54 GM133807
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA163068
Pays : United States
Organisme : NIMHD NIH HHS
ID : U54 MD007587
Pays : United States
Organisme : NIMHD NIH HHS
ID : G12 MD007579
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM096955
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA163071
Pays : United States
Organisme : NCI NIH HHS
ID : F31 CA247459
Pays : United States
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