Journal article
Estrogen receptor alpha drives proliferation in PTEN-deficient prostate carcinoma by stimulating survival signaling, MYC expression and altering glucose sensitivity
I Takizawa, MG Lawrence, P Balanathan, R Rebello, HB Pearson, E Garg, J Pedersen, N Pouliot, R Nadon, MJ Watt, RA Taylor, P Humbert, I Topisirovic, O Larsson, GP Risbridger, L Furic
Oncotarget | Published : 2015
Abstract
While high doses of estrogen, in combination with androgens, can initiate prostate cancer (PCa) via activation of the estrogen receptor α (ERα), the role of ERα in PCa cells within established tumors is largely unknown. Here we show that expression of ERα is increased in high grade human PCa. Similarly, ERα is elevated in mouse models of aggressive PCa driven by MYC overexpression or deletion of PTEN. Within the prostate of PTEN-deficient mice, there is a progressive pattern of ERα expression: low in benign glands, moderate in tumors within the dorsal, lateral and ventral lobes, and high in tumors within the anterior prostate. This expression significantly correlates with the proliferation m..
View full abstractGrants
Awarded by Australian Research Council
Funding Acknowledgements
Funding was obtained from the National Health and Medical Research Council (Enabling Grant to APCB: 614296, Fellowship to GR: 1002648, Project Grant: 1020959, Fellowship to ML: 1035721, Fellowship to MW: 606460), Prostate Cancer Foundation of Australia (Infrastructure grant to APCB; Movember Young Investigator Grants to RT, ML, LF and HP) and Australian Research Council (DECRA Fellowship to LF: DE120100434). EG supported by MICRTP Studentship. OL is funded by the Swedish Research Council, the Swedish Cancer Foundation and the Wallenberg Academy Fellows program. HP is supported by a Richard Pratt Foundation Fellowship for Prostate Cancer Research.