ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
The INAVA mRNA in Extracellular Vesicles Activates Normal Ovarian Fibroblasts by Phosphorylation-Ubiquitylation Crosstalk of HMGA2.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Proximity labeling at H3K9me3 reveals VRK-1 regulate global chromatin distribution inbioRxiv : the preprint server for biology · 2026Article
- The Expression and Clinical Significance of C1orf106 in Low-Grade Serous Ovarian Cancer.The journal of obstetrics and gynaecology research · 2025Article
- The INAVA mRNA in Extracellular Vesicles Activates Normal Ovarian Fibroblasts by Phosphorylation-Ubiquitylation Crosstalk of HMGA2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
Ovarian cancer is an aggressive gynecological tumor usually diagnosed with widespread metastases. Extracellular vesicles (EVs), though recognized as important mediators of tumor metastasis, have received limited attention into their specific functions via the mRNA profiling. Here it is reported elevated expression and selective enrichment of INAVA mRNA in both plasma- and tissue-derived EVs from ovarian cancer patients, which is positively correlated with distant metastasis and poor prognosis. Functionally, INAVA mRNA, upon uptake and translation, activates normal ovarian fibroblasts (NOFs) and drives extensive peritoneum metastasis in the orthotopic xenograft mouse model. Mechanistically, INAVA competitively binds with high mobility group protein A2 (HMGA2) and consequently inhibit its interaction with vaccinia-related kinase 1 (VRK1), leading to reduced HMGA2 phosphorylation on Ser105. Interestingly, this inhibitory phosphorylation stabilizes HMGA2 via blocking tripartite motif-containing 21 (TRIM21) -mediated K48-linked ubiquitylation, and ultimately enhances the transcription of STAT3 to activate NOFs. Lastly, a cell-permeable peptide that disrupts the INAVA-HMGA2 interaction leads to attenuated NOF activation and provides a promising strategy for ovarian cancer therapy.
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Registered trials
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