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Marine-Derived Enteromorpha prolifera Polysaccharides Suppress Castration-Resistant Prostate Cancer via Akt1 Inhibition.

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The journal of gene medicine 2025 Vol.27(9) p. e70038
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Lin P, Yao N, Lin T, Zou Y, Lin W, Lin Y

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Prostate cancer remains a leading cause of cancer-related mortality, with castration-resistant and metastatic forms posing significant therapeutic challenges.

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APA Lin P, Yao N, et al. (2025). Marine-Derived Enteromorpha prolifera Polysaccharides Suppress Castration-Resistant Prostate Cancer via Akt1 Inhibition.. The journal of gene medicine, 27(9), e70038. https://doi.org/10.1002/jgm.70038
MLA Lin P, et al.. "Marine-Derived Enteromorpha prolifera Polysaccharides Suppress Castration-Resistant Prostate Cancer via Akt1 Inhibition.." The journal of gene medicine, vol. 27, no. 9, 2025, pp. e70038.
PMID 40974050 ↗
DOI 10.1002/jgm.70038

Abstract

Prostate cancer remains a leading cause of cancer-related mortality, with castration-resistant and metastatic forms posing significant therapeutic challenges. Marine-derived polysaccharides from Enteromorpha prolifera (EP) have emerged as promising anticancer agents due to their unique bioactive properties. In this study, we investigated the antitumor effects of EP on prostate cancer cells and elucidated its underlying molecular mechanisms. EP demonstrated selective cytotoxicity against aggressive DU145 prostate cancer cells. Mechanistically, EP induced G1/S cell cycle arrest, suppressed DNA synthesis, and inhibited epithelial-mesenchymal transition. Cellular thermal shift assays confirmed EP-Akt1 interaction, increasing the thermal stability of Akt1. These findings establish EP as a novel Akt1-targeting agent that simultaneously blocks proliferative and metastatic pathways in prostate cancer. In conclusion, our results highlight the therapeutic potential of EP as a multitargeted, marine-derived compound for prostate cancer treatment.

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