ArticleJournal of nanobiotechnology2026
Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundPlatinum-based chemotherapy for ovarian cancer is frequently compromised by the development of drug resistance, which is often accompanied by an immunosuppressive tumor microenvironment. The molecular mechanisms linking cisplatin resistance to immune evasion remain poorly understood, hindering the development of effective combination therapies.
resultsThis study revealed that cisplatin-induced resistance and immunosuppression were driven by reduced N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification, which produced two distinct unfavorable effects: (1) activation of the DNA damage repair pathway, thereby promoting cisplatin resistance; and (2) activation of the TGF-β pathway through enhanced translation efficiency of Gdf6 and Inhba. Mechanistically, NAT10 bound to ribosomal proteins RPS3 and RPS6, creating a steric barrier that inhibited the loading of ac4C-modified mRNAs onto ribosomes. Elevated TGF-β signaling increased the infiltration of myeloid-derived suppressor cells, M2 macrophages, exhausted CD8 + T cells, and regulatory T cells within the tumor microenvironment. To target this pathway, we developed a luteinizing hormone-releasing hormone (LHRH) receptor-targeted nanodelivery system (NanoTi) for a TGF-β inhibitor, which synergized with cisplatin to achieve superior antitumor efficacy by effectively reversing the immunosuppressive microenvironment.
conclusionsOur findings suggest that cisplatin-induced NAT10/ac4C downregulation may contribute to platinum resistance and immunosuppression in ovarian cancer, and targeted TGF-β inhibition reverses cisplatin-induced immunosuppression in preclinical ovarian cancer models.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.