Faculty Opinions recommendation of β-Catenin, a Sox2 binding partner, regulates the DNA binding and transcriptional activity of Sox2 in breast cancer cells.

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.

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Endocrine Disruptor Agent Nonyl Phenol Exerts An Estrogen-like Transcriptional Activity on Estrogen Receptor Positive Breast Cancer Cells

Current Medicinal Chemistry ◽

10.2174/09298673113209990169 ◽

2014 ◽

Vol 21 (5) ◽

pp. 630-640 ◽

Cited By ~ 15

Author(s):

A.A. Amaro ◽

A.I. Esposito ◽

V. Mirisola ◽

A. Mehilli ◽

C. Rosano ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cancer Cells ◽

Endocrine Disruptor ◽

Breast Cancer Cells ◽

Transcriptional Activity ◽

Nonyl Phenol ◽

Estrogen Receptor Positive ◽

Positive Breast Cancer

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Multifunctional Carbon dot anchored halloysite nanotube: nanovehicle for cisplatin drug release, cytotoxicity on breast cancer cells and DNA binding studies

Chemical Data Collections ◽

10.1016/j.cdc.2021.100827 ◽

2022 ◽

pp. 100827

Author(s):

M.K. Prashanth ◽

K. Chaitra ◽

Prakash Krishnaiah ◽

K.N. Prashanth ◽

K. Yogesh kumar ◽

...

Keyword(s):

Breast Cancer ◽

Dna Binding ◽

Drug Release ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Binding Studies ◽

Halloysite Nanotube ◽

Carbon Dot ◽

Dna Binding Studies

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Oleic acid induces ERK1/2 activation and AP-1 DNA binding activity through a mechanism involving Src kinase and EGFR transactivation in breast cancer cells

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2008.08.003 ◽

2008 ◽

Vol 294 (1-2) ◽

pp. 81-91 ◽

Cited By ~ 60

Author(s):

Adriana Soto-Guzman ◽

Teresa Robledo ◽

Mario Lopez-Perez ◽

Eduardo Perez Salazar

Keyword(s):

Breast Cancer ◽

Oleic Acid ◽

Dna Binding ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Src Kinase ◽

Binding Activity ◽

Egfr Transactivation ◽

Dna Binding Activity

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Screening antiproliferative drug for breast cancer from bisbenzylisoquinoline alkaloid tetrandrine and fangchinoline derivatives by targeting BLM helicase

BMC Cancer ◽

10.1186/s12885-019-6146-7 ◽

2019 ◽

Vol 19 (1) ◽

Author(s):

Wangming Zhang ◽

Shuang Yang ◽

Jinhe Liu ◽

Linchun Bao ◽

He Lu ◽

...

Keyword(s):

Breast Cancer ◽

Dna Binding ◽

Small Molecules ◽

Cancer Cells ◽

Small Molecule ◽

Breast Cancer Cells ◽

Dna Unwinding ◽

Protein Levels ◽

Blm Helicase ◽

Bisbenzylisoquinoline Alkaloids

Abstract Background The high expression of BLM (Bloom syndrome) helicase in tumors involves its strong association with cell expansion. Bisbenzylisoquinoline alkaloids own an antitumor property and have developed as candidates for anticancer drugs. This paper aimed to screen potential antiproliferative small molecules from 12 small molecules (the derivatives of bisbenzylisoquinoline alkaloids tetrandrine and fangchinoline) by targeting BLM642–1290 helicase. Then we explore the inhibitory mechanism of those small molecules on proliferation of MDA-MB-435 breast cancer cells. Methods Fluorescence polarization technique was used to screen small molecules which inhibited the DNA binding and unwinding of BLM642–1290 helicase. The effects of positive small molecules on the ATPase and conformation of BLM642–1290 helicase were studied by the malachite green-phosphate ammonium molybdate colorimetry and ultraviolet spectral scanning, respectively. The effects of positive small molecules on growth of MDA-MB-435 cells were studied by MTT method, colony formation and cell counting method. The mRNA and protein levels of BLM helicase in the MDA-MB-435 cells after positive small molecule treatments were examined by RT-PCR and ELISA, respectively. Results The compound HJNO (a tetrandrine derivative) was screened out which inhibited the DNA binding, unwinding and ATPase of BLM642–1290 helicase. That HJNO could bind BLM642–1290helicase to change its conformationcontribute to inhibiting the DNA binding, ATPase and DNA unwinding of BLM642–1290 helicase. In addition, HJNO showed its inhibiting the growth of MDA-MB-435 cells. The values of IC50 after drug treatments for 24 h, 48 h and 72 h were 19.9 μmol/L, 4.1 μmol/L and 10.9 μmol/L, respectively. The mRNA and protein levels of BLM helicase in MDA-MB-435 cells increased after HJNO treatment. Those showed a significant difference (P < 0.05) compared with negative control when the concentrations of HJNO were 5 μmol/L and 10 μmol/L, which might contribute to HJNO inhibiting the DNA binding, ATPase and DNA unwinding of BLM helicase. Conclusion The small molecule HJNO was screened out by targeting BLM642–1290 helicase. And it showed an inhibition on MDA-MB-435 breast cancer cells expansion.

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Identification of a novel estrogen receptor β1 binding partner, inhibitor of differentiation-1, and role of ERβ1 in human breast cancer cells

Cancer Letters ◽

10.1016/j.canlet.2009.01.008 ◽

2009 ◽

Vol 278 (2) ◽

pp. 210-219 ◽

Cited By ~ 28

Author(s):

Li Chen ◽

Juhui Qiu ◽

Cheng Yang ◽

Xinghua Yang ◽

Xianchun Chen ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Human Breast Cancer Cells ◽

Human Breast ◽

Binding Partner ◽

Inhibitor Of Differentiation 1

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MiR-873 regulates ERα transcriptional activity and tamoxifen resistance via targeting CDK3 in breast cancer cells

Oncogene ◽

10.1038/onc.2014.430 ◽

2014 ◽

Vol 34 (30) ◽

pp. 3895-3907 ◽

Cited By ~ 49

Author(s):

J Cui ◽

Y Yang ◽

H Li ◽

Y Leng ◽

K Qian ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Transcriptional Activity ◽

Tamoxifen Resistance

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Unique Roles of p160 Coactivators for Regulation of Breast Cancer Cell Proliferation and Estrogen Receptor-α Transcriptional Activity

Endocrinology ◽

10.1210/en.2008-1001 ◽

2008 ◽

Vol 150 (4) ◽

pp. 1588-1596 ◽

Cited By ~ 46

Author(s):

Sudipan Karmakar ◽

Estrella A. Foster ◽

Carolyn L. Smith

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Estrogen Receptor ◽

Mrna Expression ◽

Cancer Cells ◽

Small Interfering Rna ◽

Breast Cancer Cells ◽

Transcriptional Activity ◽

Interfering Rna ◽

Mcf 7

Each of the three members of the p160 steroid receptor coactivator (SRC) family of coactivators (SRC-1, SRC-2 and SRC-3) stimulates estrogen receptor (ER)-α function in trans-activation assays. Consequently, we sought to elucidate their contributions to the ER-regulated processes of cell proliferation, apoptosis, and the expression of ERα target genes in MCF-7 breast cancer cells. The small interfering RNA depletion of SRC-2 or SRC-3 but not SRC-1 inhibited growth of MCF-7 cells, and this was reflected in decreased cell cycle progression and increased apoptosis in SRC-2- or SRC-3-depleted cells as well as a reduction in ERα transcriptional activity measured on a synthetic reporter gene. However, only SRC-3 depletion blocked estradiol stimulated cell proliferation. Depletion of SRC-1 did not affect these events, and together this reveals functional differences between each of the three SRC family coactivators. Regulation of the endogenous ERα target gene, c-myc was not affected by depletion of any of the p160 coactivators although depletion of each of them decreased pS2 mRNA expression in estradiol-treated MCF-7 cells. Moreover, progesterone receptor and cyclin D1 gene expression were decreased in SRC-3 small interfering RNA-treated cells. Expression of mRNA and protein levels for the antiapoptotic gene, Bcl-2 was dependent on SRC-3 expression, whereas Bcl-2 protein but not mRNA expression also was sensitive to SRC-1 depletion. Together these data indicate that the closely related p160 coactivators are not functionally redundant in breast cancer cells because they play gene-specific roles in regulating mRNA and protein expression, and they therefore are likely to make unique contributions to breast tumorigenesis.

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