ERa-Dependent E2F Transcription Can Mediate Resistance to Estrogen Deprivation in Human Breast Cancer

نویسندگان

  • Todd W. Miller
  • Justin M. Balko
  • Emily M. Fox
  • Zara Ghazoui
  • Anita Dunbier
  • Helen Anderson
  • Mitch Dowsett
  • Aixiang Jiang
  • R. Adam Smith
  • Sauveur-Michel Maira
  • H. Charles Manning
  • Ana M. González-Angulo
  • Gordon B. Mills
  • Catherine Higham
  • Siprachanh Chanthaphaychith
  • Maria G. Kuba
  • William R. Miller
  • Yu Shyr
  • Carlos L. Arteaga
چکیده

Authors' Affiliations: Departments of Cancer Biology, Medicine, Biostatistics, Radiology and Radiological Sciences, and Pathology; Breast Cancer Research Program, Vanderbilt-Ingram Cancer Center; Institute of Imaging Sciences, Vanderbilt University, Nashville, Tennessee; Breakthrough Breast Cancer Centre, Institute of Cancer Research, and Academic Department of Biochemistry, Royal Marsden Hospital, London, UK; Novartis Institute for Biomedical Research, Oncology Disease Area, Basel, Switzerland; Departments of Breast Medical Oncology and Systems Biology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas; Breast Research Group, University of Edinburgh, Edinburgh, UK Note: Supplementary data for this article are available at Cancer Discovery Online (http://www.cancerdiscovery.aacrjournals.org).

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

ERα-dependent E2F transcription can mediate resistance to estrogen deprivation in human breast cancer.

Most estrogen receptor α (ER)-positive breast cancers initially respond to antiestrogens, but many eventually become estrogen-independent and recur. We identified an estrogen-independent role for ER and the CDK4/Rb/E2F transcriptional axis in the hormone-independent growth of breast cancer cells. ER downregulation with fulvestrant or small interfering RNA (siRNA) inhibited estrogen-independent ...

متن کامل

BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists.

Estrogen antagonists are universally employed in the breast cancer therapy, although antagonist therapy is limited by the inevitable development of cellular resistance. The molecular mechanisms by which these agents inhibit cellular proliferation in breast cancer cells are not fully defined. Recent studies have shown the involvement of the E2F pathway in tamoxifen-induced growth arrest. We show...

متن کامل

Molecular and Cellular Pathobiology Estrogen-Dependent Gene Transcription in Human Breast Cancer Cells Relies upon Proteasome-Dependent Monoubiquitination of Histone H2B

The estrogen receptor-a (ERa) determines the phenotype of breast cancers where it serves as a positive prognostic indicator. ERa is a well-established target for breast cancer therapy, but strategies to target its function remain of interest to address therapeutic resistance and further improve treatment. Recent findings indicate that proteasome inhibition can regulate estrogen-induced transcri...

متن کامل

Endocrine therapy resistance can be associated with high estrogen receptor a (ERa) expression and reduced ERa phosphorylation in breast cancer models

Hormone-dependent estrogen receptor (ER)-positive breast cancer cells may adapt to low estrogen environments such as produced by aromatase inhibitors. In many instances, cells become insensitive to the effects of estrogen but may still retain dependence on ER. We have investigated the expression, function, and activation of ERa in two endocrine-resistant MCF-7 models to identify mechanisms that...

متن کامل

Apigenin inhibits antiestrogen-resistant breast cancer cell growth through estrogen receptor-A-dependent and estrogen receptor-A-independent mechanisms

Breast cancer resistance to the antiestrogens tamoxifen (OHT) and fulvestrant is accompanied by alterations in both estrogen-dependent and estrogen-independent signaling pathways. Consequently, effective inhibition of both pathways may be necessary to block proliferation of antiestrogen-resistant breast cancer cells. In this study, we examined the effects of apigenin, a dietary plant flavonoid ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2011