作者: Momoe Itsumi , Masaki Shiota , Akira Yokomizo , Eiji Kashiwagi , Ario Takeuchi
DOI: 10.1530/JME-13-0024
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摘要: Androgen receptor (AR) signaling is critical for the tumorigenesis and development of prostate cancer, as well progression to castration-resistant cancer. We previously showed that heterochromatin protein 1 (HP1) β isoform plays a role in transactivation AR an coactivator promotes cancer cell proliferation. However, roles other HP1 isoforms, HP1α HP1γ, expression remain unclear. Here, we found knockdown but not HP1α, reduced proliferation by inducing cycle arrest at G1 phase LNCaP cells. Conversely, overexpression full-length its C-terminal deletion mutant increased growth, whereas HP1γ had no effect. Similarly, promoted 22Rv1 CxR cells, derivative. Taken together, isoforms distinctly augment growth Therefore, silencing HP1β may be promising therapeutic strategy treatment