The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Distinct Transcriptional Programs Mediated by the Ligand-Dependent Full-Length Androgen Receptor and Its Splice Variants in Castration-Resistant Prostate Cancer
Open accessAbstract
Continued androgen receptor (AR) signaling is an established mechanism underlying castration-resistant prostate cancer (CRPC), and suppression of androgen receptor signaling remains a therapeutic goal of CRPC therapy. Constitutively active androgen receptor splice variants (AR-Vs) lack the androgen receptor ligand-binding domain (AR-LBD), the intended target of androgen deprivation therapies including CRPC therapies such as abiraterone and MDV3100. While the canonical full-length androgen receptor (AR-FL) and AR-Vs are both increased in CRPCs, their expression regulation, associated transcriptional programs, and functional relationships have not been dissected. In this study, we show that suppression of ligand-mediated AR-FL signaling by targeting AR-LBD leads to increased AR-V expression in two cell line models of CRPCs. Importantly, treatment-induced AR-Vs activated a distinct expression signature enriched for cell-cycle genes without requiring the presence of AR-FL. Conversely, activation of AR-FL signaling suppressed the AR-Vs signature and activated expression programs mainly associated with macromolecular synthesis, metabolism, and differentiation. In prostate cancer cells and CRPC xenografts treated with MDV3100 or abiraterone, increased expression of two constitutively active AR-Vs, AR-V7 and ARV567ES, but not AR-FL, paralleled increased expression of the androgen receptor–driven cell-cycle gene UBE2C. Expression of AR-V7, but not AR-FL, was positively correlated with UBE2C in clinical CRPC specimens. Together, our findings support an adaptive shift toward AR-V–mediated signaling in a subset of CRPC tumors as the AR-LBD is rendered inactive, suggesting an important mechanism contributing to drug resistance to CRPC therapy. Cancer Res; 72(14); 3457–62. ©2012 AACR.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Abiraterone and Increased Survival in Metastatic Prostate Cancer
de Bono, J. S., Logothetis, C. J., Molina, A., Fizazi, K., North, S., Chu, L., Chi, K. N., Jones, R. J., Goodman, O. B., Saad, F., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1014618 · Cited by 4,407 · cited 1×
“Nevertheless, themajority of patients progress shortly after treatment, again with reactivated androgen receptor signaling (4, 5).”
Development of a second-generation antiandrogen for treatment of advanced prostate cancer.
Tran, C., Ouk, S., Clegg, N. J., Chen, Y., Watson, P. A., Arora, V., Wongvipat, J., Smith-Jones, P. M., Yoo, D., Kwon, A., et al. (2009) · Science · doi:10.1126/science.1168175 · Cited by 2,292
Hu, R., Dunn, T. A., Wei, S., Isharwal, S., Veltri, R. W., Humphreys, E., Han, M., Partin, A. W., Vessella, R. L., Isaacs, W. B., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-2764 · Cited by 1,077
Self-citationAndrogen Receptor Regulates a Distinct Transcription Program in Androgen-Independent Prostate Cancer
Wang, Q., Li, W., Zhang, Y., Yuan, X., Xu, K., Yu, J., Chen, Z., Beroukhim, R., Wang, H., Lupien, M., et al. (2009) · Cell · doi:10.1016/j.cell.2009.04.056 · Cited by 902
Guo, Z., Yang, X., Sun, F., Jiang, R., Linn, D. E., Chen, H., Chen, H., Kong, X., Melamed, J., Tepper, C. G., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-3795 · Cited by 880
Self-citationDehm, S. M., Schmidt, L. J., Heemers, H. V., Vessella, R. L., & Tindall, D. J. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-0594 · Cited by 834
Sun, S., Sprenger, C. C. T., Vessella, R. L., Haugk, K., Soriano, K., Mostaghel, E. A., Page, S. T., Coleman, I. M., Nguyen, H. M., Sun, H., et al. (2010) · Journal of Clinical Investigation · doi:10.1172/jci41824 · Cited by 748
Self-citationWatson, P. A., Chen, Y. F., Balbas, M. D., Wongvipat, J., Socci, N. D., Viale, A., Kim, K., & Sawyers, C. L. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1012443107 · Cited by 639
Mostaghel, E. A., Marck, B. T., Plymate, S. R., Vessella, R. L., Balk, S., Matsumoto, A. M., Nelson, P. S., & Montgomery, R. B. (2011) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-11-0728 · Cited by 588
Self-citation
Cited by
AR-V7 and Resistance to Enzalutamide and Abiraterone in Prostate Cancer
Antonarakis, E. S., Lu, C., Wang, H., Luber, B., Nakazawa, M., Roeser, J. C., Chen, Y., Mohammad, T. A., Chen, Y., Fedor, H. L., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1315815 · Cited by 2,710
Self-citationAttard, G., Parker, C., Eeles, R. A., Schröder, F., Tomlins, S. A., Tannock, I., Drake, C. G., & de Bono, J. S. (2016) · The Lancet · doi:10.1016/s0140-6736(14)61947-4 · Cited by 905
Karantanos, T., Corn, P. G., & Thompson, T. C. (2013) · Oncogene · doi:10.1038/onc.2013.206 · Cited by 866
PROTAC-induced BET protein degradation as a therapy for castration-resistant prostate cancer
Raina, K., Lu, J., Qian, Y., Altieri, M., Gordon, D., Rossi, A. M. K., Wang, J., Chen, X., Dong, H., Siu, K., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1521738113 · Cited by 852
Azad, A. A., Volik, S. V., Wyatt, A. W., Haegert, A., Le Bihan, S., Bell, R. H., Anderson, S. A., McConeghy, B., Shukin, R., Bazov, J., et al. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2666 · Cited by 478
Metadata
- Authors
- Hu, R., Lu, C., Mostaghel, E. A., Yegnasubramanian, S., Gurel, M., Tannahill, C., Edwards, J., Isaacs, W. B., Nelson, P. S., Bluemn, E., Plymate, S. R., & Luo, J.
- Venue
- Cancer Research
- Published
- 2012-07-15
- Volume
- 72
- Issue
- 14
- Pages
- 3457-3462
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- OpenAlex
- W1999343166
- Cited by
- 583
- References
- 19
- FWCI
- 41.74
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Distinct Transcriptional Programs Mediated by the Ligand-Dependent Full-Length Androgen Receptor and Its Splice Variants in Castration-Resistant Prostate Cancer. https://app.cochat.ai/papers/10.1158/0008-5472.can-11-3892
- The paper
- Hu, R., Lu, C., Mostaghel, E. A., Yegnasubramanian, S., Gurel, M., Tannahill, C., Edwards, J., Isaacs, W. B., Nelson, P. S., Bluemn, E., Plymate, S. R., & Luo, J. (2012). Distinct Transcriptional Programs Mediated by the Ligand-Dependent Full-Length Androgen Receptor and Its Splice Variants in Castration-Resistant Prostate Cancer. Cancer Research. https://doi.org/10.1158/0008-5472.can-11-3892
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
