The HER2/Grb2/Akt pathway regulates the DNA binding activity of AP-1 in breast cancer cells

2004 ◽  
Author(s):  
Edgar Mendoza-Gamboa ◽  
Doris Siwak ◽  
Ana Tari
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Binding Activity ◽  
Akt Pathway ◽  
Dna Binding Activity

A transcriptional repressive role for epithelial-specific ETS factor ELF3 on oestrogen receptor alpha in breast cancer cells

2016 ◽  
Vol 473 (8) ◽  
pp. 1047-1061 ◽  
Author(s):  
Vijaya Narasihma Reddy Gajulapalli ◽  
Venkata Subramanyam Kumar Samanthapudi ◽  
Madhusudana Pulaganti ◽  
Saratchandra Singh Khumukcham ◽  
Vijaya Lakhsmi Malisetty ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Dna Binding ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Transcriptional Activity ◽  
Ectopic Expression ◽  
Binding Activity ◽  
Dna Binding Activity

Oestrogen receptor-α (ERα) is a ligand-dependent transcription factor that primarily mediates oestrogen (E2)-dependent gene transcription required for mammary gland development. Coregulators critically regulate ERα transcription functions by directly interacting with it. In the present study, we report that ELF3, an epithelial-specific ETS transcription factor, acts as a transcriptional repressor of ERα. Co-immunoprecipitation (Co-IP) analysis demonstrated that ELF3 strongly binds to ERα in the absence of E2, but ELF3 dissociation occurs upon E2 treatment in a dose- and time-dependent manner suggesting that E2 negatively influences such interaction. Domain mapping studies further revealed that the ETS (E-twenty six) domain of ELF3 interacts with the DNA binding domain of ERα. Accordingly, ELF3 inhibited ERα’s DNA binding activity by preventing receptor dimerization, partly explaining the mechanism by which ELF3 represses ERα transcriptional activity. Ectopic expression of ELF3 decreases ERα transcriptional activity as demonstrated by oestrogen response elements (ERE)-luciferase reporter assay or by endogenous ERα target genes. Conversely ELF3 knockdown increases ERα transcriptional activity. Consistent with these results, ELF3 ectopic expression decreases E2-dependent MCF7 cell proliferation whereas ELF3 knockdown increases it. We also found that E2 induces ELF3 expression in MCF7 cells suggesting a negative feedback regulation of ERα signalling in breast cancer cells. A small peptide sequence of ELF3 derived through functional interaction between ERα and ELF3 could inhibit DNA binding activity of ERα and breast cancer cell growth. These findings demonstrate that ELF3 is a novel transcriptional repressor of ERα in breast cancer cells. Peptide interaction studies further represent a novel therapeutic option in breast cancer therapy.

scholarly journals Oleic acid induces migration through a FFAR1/4, EGFR and AKT-dependent pathway in breast cancer cells

2019 ◽  
Vol 8 (3) ◽  
pp. 252-265 ◽  
Author(s):  
Cleofas Marcial-Medina ◽  
Alejandra Ordoñez-Moreno ◽  
Christian Gonzalez-Reyes ◽  
Pedro Cortes-Reynosa ◽  
Eduardo Perez Salazar
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Oleic Acid ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Binding Activity ◽  
Migration And Invasion ◽  
Signal Transduction Pathways ◽  
Dna Binding Activity ◽  
Dependent Pathway

Free fatty acids (FFAs) are an energy source, and induce activation of signal transduction pathways that mediate several biological processes. In breast cancer cells, oleic acid (OA) induces proliferation, matrix metalloproteinase-9 (MMP-9) secretion, migration and invasion. However, the signal transduction pathways that mediate migration and invasion induced by OA in breast cancer cells have not been studied in detail. We demonstrate here that FFAR1 and FFAR4 mediate migration induced by OA in MDA-MB-231 and MCF-7 breast cancer cells. Moreover, OA induces migration, invasion, AKT1 and AKT2 activation, 12-LOX secretion and an increase of NFκB-DNA binding activity in breast cancer cells. Cell migration requires FFAR1, FFAR4, EGFR, AKT and PI3K activity, whereas invasion is mediated though a PI3K/Akt-dependent pathway. Furthermore, OA promotes relocalization of paxillin to focal contacts and it requires PI3K and EGFR activity, whereas NFκB-DNA binding activity requires PI3K and AKT activity.

Bovine dialyzable leukocyte extract modulates AP-1 DNA-binding activity and nuclear transcription factor expression in MCF-7 breast cancer cells

Cytotherapy ◽  
2008 ◽  
Vol 10 (2) ◽  
pp. 212-219 ◽  
Author(s):  
E. Mendoza-Gamboa ◽  
M.A. Franco-Molina ◽  
P. Zapata-Benavides ◽  
P. Castillo-Tello ◽  
M.E. Vera-García ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Binding Activity ◽  
Nuclear Transcription Factor ◽  
Dna Binding Activity ◽  
Factor Expression ◽  
Transcription Factor Expression ◽  
Mcf 7

scholarly journals α-Actinin-4 confers radioresistance coupled invasiveness in breast cancer cells through AKT pathway

2018 ◽  
Vol 1865 (1) ◽  
pp. 196-208 ◽  
Author(s):  
Sejal Desai ◽  
Amlan Barai ◽  
Amirali B. Bukhari ◽  
Abhijit De ◽  
Shamik Sen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Akt Pathway
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