We are analyzing https://link.springer.com/article/10.1186/bcr2206.

Title:
Anti-oestrogens but not oestrogen deprivation promote cellular invasion in intercellular adhesion-deficient breast cancer cells | Breast Cancer Research
Description:
Introduction Anti-oestrogens have been the mainstay of therapy in patients with oestrogen-receptor (ER) positive breast cancer and have provided significant improvements in survival. However, their benefits are limited by tumour recurrence in a significant proportion of initially drug-responsive breast cancer patients because of acquired anti-oestrogen resistance. Relapse on such therapies clinically presents as local and/or regional recurrences, frequently with distant metastases, and the prognosis for these patients is poor. The selective ER modulator, tamoxifen, classically exerts gene inhibitory effects during the drug-responsive phase in ER-positive breast cancer cells. Paradoxically, this drug is also able to induce the expression of genes, which in the appropriate cell context may contribute to an adverse cell phenotype. Here we have investigated the effects of tamoxifen and fulvestrant treatment on invasive signalling and compared this with the direct effects of oestrogen withdrawal to mimic the action of aromatase inhibitors. Methods The effect of oestrogen and 4-hydroxy-tamoxifen on the invasive capacity of endocrine-sensitive MCF-7 cells, in the presence or absence of functional E-cadherin, was determined by Matrigel invasion assays. Studies also monitored the impact of oestrogen withdrawal or treatment with fulvestrant on cell invasion. Western blotting using phospho-specific antibodies was performed to ascertain changes in invasive signalling in response to the two anti-oestrogens versus both oestradiol treatment and withdrawal. Results To the best of our knowledge, we report for the first time that tamoxifen can promote an invasive phenotype in ER-positive breast cancer cells under conditions of poor cell-cell contact and suggest a role for Src kinase and associated pro-invasive genes in this process. Our studies revealed that although this adverse effect is also apparent for further classes of anti-oestrogens, exemplified by the steroidal agent fulvestrant, it is absent during oestrogen withdrawal. Conclusions These data highlight a previously unreported effect of tamoxifen (and potentially further anti-oestrogens), that such agents appear able to induce breast cancer cell invasion in a specific context (absence of good cell-cell contacts), where these findings may have major clinical implications for those patients with tumours that have inherently poor intercellular adhesion. In such patients oestrogen deprivation with aromatase inhibitors may be more appropriate.
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Keywords {🔍}

cells, tamoxifen, cancer, breast, ecadherin, src, invasion, article, cell, expression, google, scholar, pubmed, mcf, cas, growth, sirna, activity, figure, invasive, treatment, kinase, data, oestrogen, absence, treated, cellular, adhesion, increase, fulvestrant, therapy, effects, factor, genes, cdh, patients, medium, promote, presence, receptor, significantly, hours, lobular, antioestrogens, effect, determined, authors, nicholson, signalling, studies,

Topics {✒️}

e-cadherin-mediated cell-cell adhesion e-cadherin-negative mda-mb-231 cells e-cadherin-mediated homophilic interactions e-cadherin-mediated intercellular adhesion e-cadherin-deficient mcf-7 cells er-negative mda-mb-231 cells early-stage breast cancer antibody-mediated e-cadherin disruption anti-growth factor therapies deficient e-cadherin adhesion shc-dependent erk signaling article download pdf c57bl/6j-min/+ mice rhoa-dependent actomyosin contractility good cell-cell contact peroxidise-labelled secondary antibody e-cadherin-deficient cells mi-2/nurd complex subunit tamoxifen-modulated e-cadherin expression mda-mb-231 cell invasion human e-cadherin gene e-cadherin status correlates mitogen-activated protein kinase good cell-cell contacts epidermal growth factor subsequent cell-cell adhesion poor cell-cell contact tamoxifen-induced rapid death wild-type mcf-7 cells aberrant e-cadherin expression cancers lacking e-cadherin hard-set mounting medium tamoxifen-resistant mcf-7 cells tamoxifen-induced cell invasion endocrine-sensitive mcf-7 cells tamoxifen-induced cellular invasion e-cadherin expression suppresses correlating e-cadherin expression e-cadherin immunohistochemical expression endocrine-related cancer reduced intercellular adhesion anti-hormone induced genes acquired anti-oestrogen resistance er-positive postmenopausal patients anti-phospho src kinase e-cadherin protein expression full size image early breast cancer anti-oestrogen-induced expression anti-hormone responsive cells

Questions {❓}

Cleton-Jansen AM: E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?

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WebPage:
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         Aromatase Inhibitor
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         SU6656
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         Oncology
         Surgical Oncology
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