NBPF1 acts as a tumor suppressor in prostate cancer

Rákkutatás · Prostate cancer

NBPF1 acts as a tumor suppressor in prostate cancer by regulating the PI3K/AKT pathway.

NBPF1 acts as a tumor suppressor in prostate cancer by regulating the PI3K/AKT pathway. In prostate cancer (PCa) tissues, NBPF1 is markedly down‑regulated compared with normal prostate and low expression correlates with higher Gleason grade and poorer prognosis. Gain‑of‑function experiments show that NBPF1 overexpression suppresses cell proliferation, migration and invasion, whereas knockdown produces the opposite effects. In PC3 xenografts, NBPF1 loss accelerates tumor growth. Transcriptomic profiling identifies the PI3K/AKT signaling cascade as a key downstream pathway; NBPF1 loss increases p‑AKT, MMP2 and MMP9 levels, while overexpression reduces pathway activation and protease expression. Thus, NBPF1 functions as a tumor suppressor in PCa, inhibiting progression at least partially through modulation of the PI3K/AKT pathway, and may serve as a prognostic biomarker and therapeutic target.

Understanding the molecular mechanisms that restrain prostate cancer progression is critical for developing effective therapies, especially for castration‑resistant disease. Demonstrating that NBPF1 suppresses tumor growth and invasion through the PI3K/AKT pathway suggests that restoring NBPF1 activity or targeting this pathway could improve patient outcomes.

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