The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Androgen receptor is a tumor suppressor and proliferator in prostate cancer
Open accessAbstract
Targeting androgens/androgen receptor (AR) functions via androgen deprivation therapy (ADT) remains the standard treatment for prostate cancer. However, most tumors eventually recur despite ADT. Here we demonstrate that the prostate AR may function as both a suppressor and a proliferator to suppress or promote prostate cancer metastasis. Results from orthotopically recombining stromal WPMY1 cells with epithelial PC3 prostate cancer cells in mice demonstrated that restoring AR in epithelial PC3 cells or knockdown of AR in stromal WPMY1 cells suppressed prostate cancer metastasis. Knockdown of the AR in epithelial CWR22rv1 prostate cancer cells also resulted in increased cell invasion in vitro and in vivo . Restoring AR in PC3 cells (PC3-AR9) results in decreased invasion in bone lesion assays and in vivo mouse models. Mice lacking the prostate epithelial AR have increased apoptosis in epithelial luminal cells and increased proliferation in epithelial basal cells. The consequences of these two contrasting results led to the expansion of CK5/CK8-positive intermediate cells, and mice developed larger and more invasive metastatic tumors in lymph nodes and died earlier than wild-type littermates. Mechanistic dissection suggested that androgens/AR might directly or indirectly modulate metastasis-related genes and suppression of TGFβ1 signals results in the partial inhibition of AR-mediated metastasis. Collectively, our understanding of these opposing roles of prostatic AR may revolutionize the way we combat prostate cancer, and allow the development of new and better therapies by targeting only the proliferative role of AR.
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Cites
Genome-wide association study identifies novel breast cancer susceptibility loci
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Self-citationTGF-ß Signaling in Fibroblasts Modulates the Oncogenic Potential of Adjacent Epithelia
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Self-citationMetastatic prostate cancer in a transgenic mouse.
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Akt/PKB Regulates Actin Organization and Cell Motility via Girdin/APE
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Cited by
Androgen regulation of gene expression.
(2010) · Advances in cancer research · doi:10.1016/s0065-230x(10)07005-3 · Cited by 117
The co‐chaperone p23 promotes prostate cancer motility and metastasis
Querol Cano, L., Lavery, D. N., Sin, S., Spanjaard, E., Brooke, G. N., Tilman, J. D., Abroaf, A., Gaughan, L., Robson, C. N., Heer, R., et al. (2015) · Molecular Oncology · doi:10.1016/j.molonc.2014.08.014 · Cited by 33
“This is consistent with the effects being mediated through other HSP90 client proteins or co-chaperones but does not rule out some contribution of AR, which has previously been described by other groups (Castoria et al., 2011; Castoria et al., 2003; Niu et al., 2008).”
Wen, S., Shang, Z., Zhu, S., Chang, C., & Niu, Y. (2013) · The Prostate · doi:10.1002/pros.22676 · Cited by 32
Self-citation
Metadata
- Authors
- Niu, Y., Altuwaijri, S., Lai, K.-P., Wu, C.-T., Ricke, W. A., Messing, E. M., Yao, J., Yeh, S., & Chang, C.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2008-08-26
- Volume
- 105
- Issue
- 34
- Pages
- 12182-12187
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2100465174
- Cited by
- 256
- References
- 36
- FWCI
- 16.14
- Type
- journal article
- Language
- en
- Open access
- bronze
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