ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Nanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.
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 5 papers.
What it found
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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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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.
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Who cites it
5 citing papers in PubMed.
- HMGCR-Driven Cholesterol Metabolism Promotes Osteoarthritis Progression by Accelerating Synovial Fibroblast Senescence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Patient-Derived 3D-Bioprinted Intrahepatic Cholangiocarcinoma Models Recapitulate Tumor Autologous Traits and Predict Personalized Adjuvant Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Gene Therapy for the Treatment of Osteoarthritis: Advances and Prospective.Current pharmaceutical design · 2026Review
- ERK1/2 Signaling in Intrahepatic Cholangiocarcinoma: From Preclinical Advances to Therapeutic Strategies.Biology · 2025Review
- Nanosize Non-Viral Gene Therapy Reverses Senescence Reprograming Driven by PBRM1 Deficiency to Suppress iCCA Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Polybromo-1 (PBRM1) serves as a crucial regulator of gene transcription in various tumors, including intrahepatic cholangiocarcinoma (iCCA). However, the exact role of PBRM1 in iCCA and the mechanism by which it regulates downstream target genes remain unclear. This research has revealed that PBRM1 is significantly downregulated in iCCA tissues, and this reduced expression is linked to aggressive clinicopathological features and a poor prognosis. Furthermore, it is demonstrated that PBRM1 can impede iCCA progression, and a gene therapy nanomedicine is developed to treat iCCA in vivo by modulating PBRM1 expression. The heightened expression of PBRM1 induces by the nanomedicine substantially inhibited tumor growth in iCCA. Conversely, the decrease in PBRM1 results in the abnormal activation of the ERK1/2 signaling pathway, a reduction in p16, p53/p21, and cellular senescence, thereby promoting iCCA advancement. Treatment with U0126, an ERK1/2 inhibitor, effectively halted iCCA progression by regulating the PBRM1-ERK1/2-cellular senescence pathway. These findings underscore the significant role of PBRM1 in controlling iCCA progression and predicting prognosis. Targeting the PBRM1-ERK1/2-cellular senescence pathway with U0126 shows promise for clinical applications in treating iCCA.
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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 Socratic graph.