Growth of hormone-dependent MCF-7 breast cancer cells is promoted by constitutive caveolin-1 whose expression is lost in an EGF-R-mediated manner during development of tamoxifen resistance

Thomas, Nicholas B. P.; Hutcheson, Iain Robert; Campbell, Lee Ann; Gee, Julia Margaret Wendy; Taylor, KM; Nicholson, Robert Ian; Gumbleton, Mark

doi:10.1007/s10549-009-0355-8

Cited by 23 publications

(23 citation statements)

References 60 publications

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“…genecards .org). In humans, benzamide exposure has been shown to result in a decreased activity and expression of MAPK1 protein (Mattingly et al 2006, Thomas et al 2010, in line with our finding for the transcript. Also mapk1 transcription showed a Ushaped type of transcription, with no significant response in the high exposure group.…”

Section: Discussionsupporting

confidence: 91%

Toxicological assessment of the anti-salmon lice drug diflubenzuron on Atlantic cod Gadus morhua

Samuelsen¹,

Erdal²,

Holmelid³

et al. 2013

Dis. Aquat. Org.

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Increasing use of the chitin synthesis inhibitor diflubenzuron against the ectoparasitic salmon louse Lepeophtheirus salmonis in marine aquaculture has raised concerns over its environmental impacts. This study evaluated how diflubenzuron affects Atlantic cod Gadus morhua, a fish species often found near Atlantic salmon Salmo salar farms, focusing on uptake kinetics and hepatic transcriptional responses. Two experiments were conducted, one time-series trial in which the fish were given a daily dose (3 mg kg −1 fish) of diflubenzuron for 14 d followed by a 3 wk depuration period, and one dose−response trial with increasing concentrations (3, 10 and 50 mg kg −1 fish). The highest diflubenzuron concentrations were found in the liver at Day 15. No detectable levels of diflubenzuron were found in liver or muscle 3 wk after the end of the treatment. At the molecular level, small effects of diflubenzuron treatment on gene transcription were observed. In the time-series experiment, the strongest effects were seen at Day 8, with 2 transcripts being upregulated (bclx2 and cpt1a) and 8 transcripts being downregulated (gstp1, gstm1, gstt1, ugt1a, nat2, cat, p53 and slc16a9a). Five transcripts (cyp3a, cpt1a, ptgs2, elovl5 and mapk1) responded significantly to diflubenzuron exposure in the dose−response experiment. This study shows that diflubenzuron can be taken up by Atlantic cod, that it is rapidly cleared from the body and that when present this pharmaceutical causes only small effects on the expression of genes involved in detoxification pathways. Taken together, our data suggest that accumulated diflubenzuron at the levels studied would have a relatively small effect on wild Atlantic cod.

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Section: Discussionsupporting

confidence: 91%

Toxicological assessment of the anti-salmon lice drug diflubenzuron on Atlantic cod Gadus morhua

Samuelsen¹,

Erdal²,

Holmelid³

et al. 2013

Dis. Aquat. Org.

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“…However, downregulation of caveolin-1 appears insufficient to confer tamoxifen resistance. It is plausible that caveolin-1 may represent a potential molecular marker for acquired endocrine resistance without playing a mechanistic role [119]. These data also suggest that caveolin-1 may facilitate non-classical cross-talk between growth factor and steroid receptor pathways.…”

Section: Er-positive Cancersmentioning

confidence: 86%

“…More recently, the transition of WT-MCF7 cells to a tamoxifen-resistant (TAM-R) phenotype has been associated with caveolin-1 suppression by hyper-activation of EGFR/ERK signalling [119]. In this model, treatment with gefitinib substantially reduces phosphorlyated-EGFR and ERK1/2 in the TAM-R cells, associated with upregulation of caveolin-1 and growth inhibition.…”

Section: Er-positive Cancersmentioning

confidence: 99%

The role of caveolin-1 in human breast cancer

Patani

Martin

Reis‐Filho

et al. 2011

Breast Cancer Res Treat

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Caveolin-1 is the essential constituent protein of specialised plasma membrane invaginations called caveolae. The unique topology of caveolin-1 facilitates the role of caveolae as molecular hubs, integrating the activity of a multitude of signalling molecules. Despite improvements in our understanding of caveolin-1 interactions and the function of caveolae, the relationship between dysfunctional caveolin-1 and tumourigenesis remains contentious. Perhaps most intriguing has been the demonstration of both oncogenic and tumour suppressor function within particular tumour types, including breast cancer. In this review, the biological and clinical relevance of caveolin-1 in human breast cancer are considered. Evidence is systematically presented for the potential tumour suppressor and oncogenic functions of caveolin-1. Specific reference is made to interactions between caveolin-1 and signalling pathways in the clinical and biological subtypes of breast cancer. Areas of controversy are discussed and technical considerations are highlighted. Translational implications and potential for specific therapeutic manipulation of caveolin-1 are evaluated in the context of evidence from in vitro and in vivo studies.

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“…Tamoxifen, a selective estrogen receptor modulator (SERM), has been the most widely used endocrine treatment in ER positive breast cancer patients for more than 30 years [3, 4]. However, primary or acquired resistance to tamoxifen results in therapeutic failure, which needs to be solved in the clinical application [5–8]. …”

Section: Introductionmentioning

confidence: 99%

Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells

et al. 2017

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Tamoxifen is still the most commonly used endocrine therapy drug for estrogen receptor (ER)-positive breast cancer patients and has an excellent outcome, but tamoxifen resistance remains a great impediment to successful treatment. Recent studies have prompted an anti-tumor effect of aspirin. Here, we demonstrated that aspirin not only inhibits the growth of ER-positive breast cancer cell line MCF-7, especially when combined with tamoxifen, but also has a potential function to overcome tamoxifen resistance in MCF-7/TAM. Aspirin combined with tamoxifen can down regulate cyclinD1 and block cell cycle in G0/G1 phase. Besides, tamoxifen alone represses c-myc, progesterone receptor (PR) and cyclinD1 in MCF-7 cell line but not in MCF-7/TAM, while aspirin combined with tamoxifen can inhibit the expression of these proteins in the resistant cell line. When knocking down c-myc in MCF-7/TAM, cells become more sensitive to tamoxifen, cell cycle is blocked as well, indicating that aspirin can regulate c-myc and cyclinD1 proteins to overcome tamoxifen resistance. Our study discovered a novel role of aspirin based on its anti-tumor effect, and put forward some kinds of possible mechanisms of tamoxifen resistance in ER-positive breast cancer cells, providing a new strategy for the treatment of ER-positive breast carcinoma.

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Growth of hormone-dependent MCF-7 breast cancer cells is promoted by constitutive caveolin-1 whose expression is lost in an EGF-R-mediated manner during development of tamoxifen resistance

Cited by 23 publications

References 60 publications

Toxicological assessment of the anti-salmon lice drug diflubenzuron on Atlantic cod Gadus morhua

Toxicological assessment of the anti-salmon lice drug diflubenzuron on Atlantic cod Gadus morhua

The role of caveolin-1 in human breast cancer

Aspirin regulation of c-myc and cyclinD1 proteins to overcome tamoxifen resistance in estrogen receptor-positive breast cancer cells

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