Restoration of cyclin D2 has an inhibitory potential on the proliferation of LNCaP cells
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 387, Issue: 1, Page: 196-201
2009
- 23Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations23
- Citation Indexes23
- 23
- CrossRef17
- Captures12
- Readers12
- 12
Article Description
Despite well known oncogenic function of G1–S cell-cycle progression, cyclin D2 ( CCND2 ) is often silenced epigenetically in prostate cancers. Here we show that CCND2 has an inhibitory potential on the proliferation of androgen receptor (AR)-dependent prostate cancer LNCaP cells. Forced expression of CCND2 suppressed the proliferative ability and induced cell death in LNCaP cells in a cdk-independent manner. Knocking down CCND2 restored the proliferation of LNCaP subclones with relatively high CCND2 expression and low proliferative profiles. Immunoprecipitation using deletion mutants of CCND2 indicated that a central domain of CCND2 is required for binding to AR. A deletion mutant lacking the central domain failed to hinder LNCaP cells. Collectively, our results indicated that CCND2 inhibits cell proliferation of AR-dependent prostate cancer through the interaction with AR. Our study suggests that restoration of CCND2 expression potentially prevents the carcinogenesis of prostate cancer, which is mostly AR-dependent in the initial settings.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X09013266; http://dx.doi.org/10.1016/j.bbrc.2009.06.146; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=67651036152&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/19577536; https://linkinghub.elsevier.com/retrieve/pii/S0006291X09013266; https://dx.doi.org/10.1016/j.bbrc.2009.06.146
Elsevier BV
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