Schematic representation of enhanced KRAS signaling through the interaction between AR-independent prostate cancer cells and AR-independent prostate cancer-associated stromal cells. (IMAGE)

Kanazawa University

Schematic representation of enhanced KRAS signaling through the interaction between AR-independent prostate cancer cells and AR-independent prostate cancer-associated stromal cells.

Caption

(A) AR signaling is suppressed by androgen deprivation therapy. (B) AR suppression leads to increased FGFR expression in prostate cancer cells. (C) AR suppression also raises CCL2 secretion from prostate cancer cells. (D) CCL2 influences AR-independent prostate cancer-associated stromal cells. (E) CCL2 stimulates FGF secretion from AR-independent prostate cancer associated cells. (F) The released FGF binds to the upregulated FGFR in prostate cancer cells. (G) FGFR signaling activates KRAS through SOS. (H) Activated KRAS enhances downstream signaling and promotes prostate cancer progression. (I) EGF is scarce in the prostate cancer microenvironment, and KRAS is less activated by EGFR signaling compared to FGFR. GEFs guanine nucleotide exchange factors, GAPs GTPase activating proteins.

Credit

Figure reproduced from Kamijima et al., Cell Death & Disease (2026), licensed under CC BY 4.0.

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