ArticleMolecular therapy. Oncology2026
Suppression of PARP1 enhances PTEN mRNA therapy in castration-resistant prostate cancer by glycolysis disruption.
Article in Molecular therapy. Oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Genetic Medicine Approaches for Tumor Suppressor Loss: Therapeutic Replacement with Self-Amplifying RNA.Pharmaceutical research · 2026Review
- A novel cancer gene therapy achieving reciprocal regulation of PTEN and PARP1 expression.Molecular therapy. Oncology · 2026Article
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Authors and funding
13 authors.
Funding
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Abstract
Current treatments for prostate cancer (PC) inevitably lead to the development of resistance to androgen deprivation therapy, resulting in the emergence of castration-resistant prostate cancer (CRPC), which is currently considered incurable. In this study, we discovered that the loss of phosphatase and tensin homolog (PTEN) function, in combination with elevated poly(ADP-ribose) polymerase 1 (PARP1) expression, significantly shortens the survival of PC patients. Motivated by this finding, we developed an RNA-based therapeutic agent consisting of PARP1-targeting small interfering RNA (siRNA) (siPARP1) and PTEN-expressing mRNA (mPTEN), which were co-encapsulated in an ionizable lipid nanoparticle, named mPsiP@miLAND. Both siPARP1 and mPTEN were shown to individually attenuate tumor cell growth. Moreover, the simultaneous regulation of these two targets nearly completely suppressed proliferation and robustly induced apoptosis and necrosis in CRPC both
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