PROCA11 early activation fuels prostate cancer neuroendocrine traits by regulating cell survival and migration.

ABSTRACT: Tumor plasticity drives the emergence of castration-resistant and neuroendocrine prostate cancer following androgen-deprivation therapy (ADT). Non-genetic determinants, including long non-coding (lnc)RNAs, preceding the acquisition of neuroendocrine traits, can disrupt androgen dependence and promote resistance. However, the precise transcriptome dynamics prior to therapy-induced neuroendocrine trans-differentiation remains unknown. Using a prostate cancer model mimicking the onset of castration-resistant and neuroendocrine phenotypes, we uncovered rapid lncRNA changes, with PROCA11 emerging as the most prominent. PROCA11 is highly expressed in advanced adenocarcinoma and neuroendocrine prostate cancer tumors. This predominantly nuclear lncRNA is rapidly activated upon hormone deple

SUBMITTER: Cipolla R 

PROVIDER: S-EPMC12664603 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature