Cell Death Dis: PLCɛ is critical to maintaining the function of AR signals in prostate cancer.

Prostate cancer (CaP), one of the most common malignancies in men, ranks first among estimated new cases in the United States and third among cancer-related deaths.
androgen-like hormones (AR) signaling path pathps play a vital role in the development of CaP.
activation of AR signals promotes cell proliferation, migration, and enditer-interstital transformation (EMT) processes, ultimately promoting tumor development.
most ar-based therapies show some efficacy in the early stages of treatment, inappropriate reactivation of ar paths inevitably leads to the emergence of drug resistance.
it is particularly important to explore how CaP cells maintain high levels of AR signaling.
the study found that PLCɛ (phospholipidase C) was highly expressed in CaP samples, and that this high expression level was closely related to the activity of ar signal transduction path.
the absence of PLC s can mediate the AMPK/ULK1 signal path path, which enhances autophagy activity, causes autophagy-mediated AR degradation and inhibits AR nuclear transport.
these effects eventually lead to the weakening of AR signals in CaP and inhibit AR-driven cell migration and invasion.
addition, a positive correlation between PLC and AR signal activity was also observed in CaP samples that were resistant to bicalutamide and in CaP cell models of AR antagonists (toner).
the absence of PLC, can lead to the inability to build CaP cell lineages resistant to AR antagonists and hinder the transfer of established cell lineages.
all, the above results show that changes in autophagy activity mediated by PLCɛ are essential for the function of AR signal transductive pathlines and the development of prostate cancer.
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