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Войти в исследования Combinatorial chemistry & high throughput screening · 2026
Natural Biopeptide Hirudin Regulates Value-Added Metastasis of Bladder Cancer Cells by Activating PID1 Expression.
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Sun Lingfeng, Yuan Lin
Аннотация
INTRODUCTION: Hirudin has natural anticoagulant and antitumor effects. This study aimed to investigate the effects of hirudin on bladder cancer cells and the regulation of the potential target PID1.
METHODS: Network pharmacology analyzed the intersecting targets of bladder cancer and hirudin drugs and performed drug-component-target association analysis. The IC50 value of hirudin in RT-112 and Scaber cells was determined by CCK8. Subsequently, 2 bladder cancer cells were treated at the IC50, and the inhibition rate of RT-112 and Scaber cells was detected using CCK8. Hirudin treatment combined with PID1 knockdown (PID1-KD) was performed to evaluate the regulatory effects of hirudin and PID1 on cell cycle progression, apoptosis, and AMPK-mTOR signaling.
RESULTS: Network pharmacology was used to analyze the intersecting targets of bladder cancer and hirudin, in which PID1 functions as a key target. Hirudin inhibited the value-added of RT- 112 and Scaber cells while promoting the apoptosis of RT-112 and Scaber cells and regulating the cell cycle of RT-112 and Scaber cells; at the same time, hirudin increased the expression level of PID1 in bladder cancer cells, and activated AMPK-mTOR signaling at the molecular level. Knockdown of PID1 partially reversed the effects induced by hirudin.
DISCUSSION: Our findings support hirudin as a potential anti-bladder cancer agent and suggest that its effects may be mediated by PID1-dependent modulation of the AMPK/mTOR pathway. Nevertheless, the study is limited by the lack of in vivo and clinical validation and by incomplete mechanistic verification.
CONCLUSION: Hirudin exerted significant inhibitory effects on bladder cancer cells, and mechanistic assays demonstrated that these effects are at least partially mediated through PID1-dependent activation of the AMPK-mTOR signaling pathway.
METHODS: Network pharmacology analyzed the intersecting targets of bladder cancer and hirudin drugs and performed drug-component-target association analysis. The IC50 value of hirudin in RT-112 and Scaber cells was determined by CCK8. Subsequently, 2 bladder cancer cells were treated at the IC50, and the inhibition rate of RT-112 and Scaber cells was detected using CCK8. Hirudin treatment combined with PID1 knockdown (PID1-KD) was performed to evaluate the regulatory effects of hirudin and PID1 on cell cycle progression, apoptosis, and AMPK-mTOR signaling.
RESULTS: Network pharmacology was used to analyze the intersecting targets of bladder cancer and hirudin, in which PID1 functions as a key target. Hirudin inhibited the value-added of RT- 112 and Scaber cells while promoting the apoptosis of RT-112 and Scaber cells and regulating the cell cycle of RT-112 and Scaber cells; at the same time, hirudin increased the expression level of PID1 in bladder cancer cells, and activated AMPK-mTOR signaling at the molecular level. Knockdown of PID1 partially reversed the effects induced by hirudin.
DISCUSSION: Our findings support hirudin as a potential anti-bladder cancer agent and suggest that its effects may be mediated by PID1-dependent modulation of the AMPK/mTOR pathway. Nevertheless, the study is limited by the lack of in vivo and clinical validation and by incomplete mechanistic verification.
CONCLUSION: Hirudin exerted significant inhibitory effects on bladder cancer cells, and mechanistic assays demonstrated that these effects are at least partially mediated through PID1-dependent activation of the AMPK-mTOR signaling pathway.