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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Molecular Cancer 1/2012

Estrogen receptor alpha deletion enhances the metastatic phenotype of Ron overexpressing mammary tumors in mice

Molecular Cancer > Ausgabe 1/2012
Aaron M Marshall, Rebecca J McClaine, Devikala Gurusamy, Jerilyn K Gray, Kara E Lewnard, Sohaib A Khan, Susan E Waltz
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-4598-11-2) contains supplementary material, which is available to authorized users.
Aaron M Marshall, Rebecca J McClaine contributed equally to this work.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

AMM and RJM were involved in the design, acquisition and analysis of the data as well as in drafting the manuscript. JKG, DG and KEL were involved in the acquisition of data. SAK was involved in the conception of the studies and the design of reagents for the ERα mouse model. SEW was involved in the conception and design of the study as well as in drafting and revising the manuscript. All authors have read and have approved the final manuscript.



The receptor tyrosine kinase family includes many transmembrane proteins with diverse physiological and pathophysiological functions. The involvement of tyrosine kinase signaling in promoting a more aggressive tumor phenotype within the context of chemotherapeutic evasion is gaining recognition. The Ron receptor is a tyrosine kinase receptor that has been implicated in the progression of breast cancer and evasion of tamoxifen therapy.


Here, we report that Ron expression is correlated with in situ, estrogen receptor alpha (ERα)-positive tumors, and is higher in breast tumors following neoadjuvant tamoxifen therapy. We also demonstrate that the majority of mammary tumors isolated from transgenic mice with mammary specific-Ron overexpression (MMTV-Ron mice), exhibit appreciable ER expression. Moreover, genetic-ablation of ERα, in the context of Ron overexpression, leads to delayed mammary tumor initiation and growth, but also results in an increased metastasis.


Ron receptor overexpression is associated with ERα-positive human and murine breast tumors. In addition, loss of ERα on a Ron overexpressing background in mice leads to the development of breast tumors which grow slower but which exhibit more metastasis and suggests that targeting of ERα, as in the case of tamoxifen therapy, may reduce the growth of Ron overexpressing breast cancers but may cause these tumors to be more metastatic.
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