. Mechanistically, the restoration of PTEN inhibited glycolysis via the PI3K-Akt signaling pathway in CRPC cells, and the silencing of PARP1 further enhanced this effect. Overall, the mPsiP@miLAND developed in this study effectively inhibited the growth of PTEN-deficient prostate tumors, providing a promising strategy to overcome CRPC by exploiting the synergistic effects of PI3K-Akt and PARP inhibition.
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Hu et al. (2026) studied this question.
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