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Cited by 260

The DOI matches its Crossref record; 67 of the 67 references it cites were found in a registry or an index.

Tamoxifen resistance in MCF7 cells promotes EMT-like behaviour and involves modulation of β-catenin phosphorylation

Hiscox, Stephen, Jiang, Wen Go, Obermeier, Kathrin, Taylor, Kathryn, Morgan, Liam, Burmi, Raj, Barrow, Denise, Nicholson, Robert I.·2006·International Journal of Cancer
DOI 10.1002/ijc.21355
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Abstract

We have previously demonstrated that, following acquisition of endocrine resistance, breast cancer cells display an altered growth rate together with increased aggressive behaviour in vitro. Since dysfunctional cell-cell adhesive interactions can promote an aggressive phenotype, we investigated the integrity of this protein complex in our breast cancer model of tamoxifen resistance. In culture, tamoxifen-resistant MCF7 (TamR) cells grew as loosely packed colonies with loss of cell-cell junctions and demonstrated altered morphology characteristic of cells undergoing epithelial-to-mesenchymal transition (EMT). Neutralising E-cadherin function promoted the invasion and inhibited the aggregation of endocrine-sensitive MCF7 cells, whilst having little effect on the behaviour of TamR cells. Additionally, TamR cells had increased levels of tyrosine-phosphorylated beta-catenin, whilst serine/threonine-phosphorylated beta-catenin was decreased. These cells also displayed loss of association between beta-catenin and E-cadherin, increased cytoplasmic and nuclear beta-catenin and elevated transcription of beta-catenin target genes known to be involved in tumour progression and EMT. Inhibition of EGFR kinase activity in TamR cells reduced beta-catenin tyrosine phosphorylation, increased beta-catenin-E-cadherin association and promoted cell-cell adhesion. In such treated cells, the association of beta-catenin with Lef-1 and the transcription of c-myc, cyclin-D1, CD44 and COX-2 were also reduced. These results suggest that homotypic adhesion in tamoxifen-resistant breast cancer cells is dysfunctional due to EGFR-driven modulation of the phosphorylation status of beta-catenin and may contribute to an enhanced aggressive phenotype and transition towards a mesenchymal phenotype in vitro.

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Cited by

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Metadata

Authors
Hiscox, S., Jiang, W. G., Obermeier, K., Taylor, K., Morgan, L., Burmi, R., Barrow, D., & Nicholson, R. I.
Venue
International Journal of Cancer
Publisher
Wiley
Published
2006-01-15
Volume
118
Issue
2
Pages
290-301
ISSN
  • 0020-7136 (ISSN-L)
  • 1097-0215
DOI
10.1002/ijc.21355
OpenAlex
W1979067350
Cited by
260
References
67
FWCI
3.11
Type
journal article
Language
en
Open access
closed

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