ARv7 promotes the escape of prostate cancer cells from androgen deprivation therapy-induced senescence by mediating the SKP2/p27 axis.

ABSTRACT:

Background

Androgen deprivation therapy (ADT) induces cellular senescence and tumor stasis, thus serving as the standard treatment for prostate cancer (PCa). However, continuous suppression of canonical androgen receptor signaling actually leads to the switch from androgen-responsive growth to androgen-independent growth, contributing to "escape" from this ADT-induced senescence (AIS) and, subsequently, the development of castration-resistant prostate cancer (CRPC). Unfortunately, the mechanism underlying this phenomenon remains elusive.

Results

In this study, we demonstrated that androgen receptor splicing variant 7 (ARv7), a dominant factor mediating abnormal AR signaling and ADT resistance, is closely associated with outgrowth from AIS of PCa cells. Mechanistically, ARv7

SUBMITTER: Zhuang D 

PROVIDER: S-EPMC11871636 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature