scholarly journals Nongenomic oestrogen signalling in oestrogen receptor negative breast cancer cells: a role for the angiotensin II receptor AT1

2006 ◽  
Vol 8 (3) ◽  
Author(s):  
Kheng Tian Lim ◽  
Niamh Cosgrave ◽  
Arnold David Hill ◽  
Leonie S Young
Keyword(s):  
Breast Cancer ◽  
Angiotensin Ii ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Angiotensin Ii Receptor ◽  
Oestrogen Signalling

scholarly journals Fulvestrant-induced expression of ErbB3 and ErbB4 receptors sensitizes oestrogen receptor-positive breast cancer cells to heregulin β1

2011 ◽  
Vol 13 (2) ◽  
Author(s):  
Iain R Hutcheson ◽  
Lindy Goddard ◽  
Denise Barrow ◽  
Richard A McClelland ◽  
Hayley E Francies ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Induced Expression ◽  
Positive Breast Cancer

Angiotensin II type 1 receptor antagonist candesartan is an angiogenic inhibitor in MDA-MB 468 human breast cancer cells

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 14114-14114
Author(s):  
D. Herr ◽  
M. Rodewald ◽  
G. Hack ◽  
R. Konrad ◽  
R. Kreienberg ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Angiotensin Ii ◽  
Cancer Cells ◽  
Tumor Angiogenesis ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Pcr Analysis ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Angiogenic Inhibitor

14114 Background: The present study examined the effect of angiotensin II on the regulation of different angiogenesis associated genes in human breast cancer cells and attempted to determine whether administration of At1R blocker candesartan could suppress the angiotensin II dependent gene regulation. Methods: Angiotensin II dependent expression of vascular endothelial growth factor (VEGF), tissue inhibitor of matrix metalloproteinases 1 (TIMP-1), and hypoxia inducible transcription factor 2alpha (HIF-2alpha) as well as administration of angiotensin II and At1R blocker candesartan was analyzed in MDA-MB 468 human breast cancer cells using immunofluorescence and TaqMan-Real-Time PCR analysis. Results: VEGF, TIMP-1, HIF-2alpha and the At1R were expressed in MDA-MB 468 human breast cancer cells. Angiotensin II significantly increased gene expression of VEGF, TIMP-1, and HIF-2alpha in these cells. This effect was completely inhibited by candesartan. Conclusion: It is hypothesized that angiotensin II is involved in regulation of tumor angiogenesis in breast cancer by regulation of angiogenesis associated genes via At1R. These findings are the first evidence for targeting tumor angiogenesis by inhibition of At1R in human breast cancer cells and may lead to new therapeutical anticancer strategies proposing administration of candesartan. No significant financial relationships to disclose.

Changing role of the oestrogen receptor in the life and death of breast cancer cells

The Breast ◽  
2003 ◽  
Vol 12 (6) ◽  
pp. 432-441 ◽  
Author(s):  
V.C Jordan ◽  
C Osipo ◽  
J.MacGregor Schafer ◽  
J.E Fox ◽  
Dong Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Life And Death ◽  
Changing Role

scholarly journals Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells

2011 ◽  
Vol 11 (7) ◽  
pp. 523-532 ◽  
Author(s):  
John J. Tyson ◽  
William T. Baumann ◽  
Chun Chen ◽  
Anael Verdugo ◽  
Iman Tavassoly ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Fate ◽  
Breast Cancer Cells ◽  
Dynamic Modelling ◽  
Oestrogen Signalling

scholarly journals Primate-specific oestrogen-responsive long non-coding RNAs regulate proliferation and viability of human breast cancer cells

Open Biology ◽  
2016 ◽  
Vol 6 (12) ◽  
pp. 150262 ◽  
Author(s):  
Chin-Yo Lin ◽  
Erica L. Kleinbrink ◽  
Fabien Dachet ◽  
Juan Cai ◽  
Donghong Ju ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Signalling Pathways ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Non Coding Rnas

Long non-coding RNAs (lncRNAs) are transcripts of a recently discovered class of genes which do not code for proteins. LncRNA genes are approximately as numerous as protein-coding genes in the human genome. However, comparatively little remains known about lncRNA functions. We globally interrogated changes in the lncRNA transcriptome of oestrogen receptor positive human breast cancer cells following treatment with oestrogen, and identified 127 oestrogen-responsive lncRNAs. Consistent with the emerging evidence that most human lncRNA genes lack homologues outside of primates, our evolutionary analysis revealed primate-specific lncRNAs downstream of oestrogen signalling. We demonstrate, using multiple functional assays to probe gain- and loss-of-function phenotypes in two oestrogen receptor positive human breast cancer cell lines, that two primate-specific oestrogen-responsive lncRNAs identified in this study (the oestrogen-repressed lncRNA BC041455, which reduces cell viability, and the oestrogen-induced lncRNA CR593775, which increases cell viability) exert previously unrecognized functions in cell proliferation and growth factor signalling pathways. The results suggest that oestrogen-responsive lncRNAs are capable of altering the proliferation and viability of human breast cancer cells. No effects on cellular phenotypes were associated with control transfections. As heretofore unappreciated components of key signalling pathways in cancers, including the MAP kinase pathway, lncRNAs hence represent a novel mechanism of action for oestrogen effects on cellular proliferation and viability phenotypes. This finding warrants further investigation in basic and translational studies of breast and potentially other types of cancers, has broad relevance to lncRNAs in other nuclear hormone receptor pathways, and should facilitate exploiting and targeting these cell viability modulating lncRNAs in post-genomic therapeutics.

Xenoestrogens and the induction of proliferative effects in breast cancer cells via direct activation of oestrogen receptor α

2004 ◽  
Vol 21 (2) ◽  
pp. 134-144 ◽  
Author(s):  
A. G. Recchia ◽  
A. Vivacqua ◽  
S. Gabriele ◽  
A. Carpino ◽  
G. Fasanella ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Direct Activation ◽  
Oestrogen Receptor Α

scholarly journals Conjugation of palbociclib with MHI-148 has an increased cytotoxic effect for breast cancer cells and an altered mechanism of action

2021 ◽  
Author(s):  
Euphemia Leung ◽  
Petr Tomek ◽  
Moana Tercel ◽  
Johannes Reynisson ◽  
Thomas In Hyeup Park ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Endocrine Therapy ◽  
Mechanism Of Action ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Cytotoxic Effect ◽  
Near Infrared ◽  
Triple Negative ◽  
Mammalian Cell Lines

The CDK4/6 inhibitor palbociclib, combined with endocrine therapy, has been shown to be effective in postmenopausal women with oestrogen receptor positive, HER2-negative advanced or metastatic breast cancer. However, palbociclib is not as effective in the highly aggressive triple-negative breast cancer that lacks sensitivity to chemotherapy or endocrine therapy. We hypothesized that conjugation of the near-infrared dye MHI-148 with palbociclib can produce a potential theranostic in triple-negative as well as oestrogen receptor positive breast cancer cells. In our study, the conjugate was found to have enhanced activity in all mammalian cell lines tested in vitro. However, the conjugate was cytotoxic and did not induce G1 cell cycle arrest in breast cancer cells suggesting the mechanism of action differed from the parent compound palbociclib. The study highlights the importance of investigating the mechanism of conjugates of near-infrared dyes to therapeutic compounds as conjugation can potentially result in a change of mechanism or target, with an enhanced cytotoxic effect in this case.

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