Fig. 8
From: A novel lncRNA FLJ promotes castration resistance in prostate cancer through AR mediated autophagy
Schematic diagram displays the function of FLJ in CRPC. Elevated androgen receptor (AR) levels in castration-resistant prostate cancer (CRPC) stimulate the expression of a novel long non-coding RNA FLJ. FLJ inhibits AR translocation to the nucleus, disrupting the conventional androgen-dependent survival pathway. Concurrently, FLJ stabilizes AR protein in the cytoplasm by preventing its degradation. Additionally, FLJ induces autophagy through AR-mediated low-dose androgen stimulation, promoting CRPC cell proliferation and re-sensitizing these cells to castration-mimetic conditions and anti-androgen therapies in vitro