ArticleACS nano2016
Gold Nanoparticle Reprograms Pancreatic Tumor Microenvironment and Inhibits Tumor Growth.
Article in ACS nano, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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.
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
72 citing papers in PubMed, 155 citations in OpenAlex.
- Review
- Ferroptosis-Based Nanotherapy for Pancreatic Ductal Adenocarcinoma Through Glutathione Depletion and Iron Accumulation.International journal of nanomedicine · 2026Review
- Nanomedicine for targeting cancer-associated fibroblasts in cancer therapy.Theranostics · 2026Review
- Exploring Morphology of Thermoplasmonic Nanoparticles to Synergize Immunotherapeutic Fibroblast Activation Protein-Positive Cell Sensitization and Photothermal Therapy.Small science · 2025Article
- Application of nanomedicines in tumor immunotherapy.Journal of molecular cell biology · 2025Review
- Harnessing the Power of Nanocarriers to Exploit the Tumor Microenvironment for Enhanced Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Interrogation of the tumor microenvironment by nanoparticles.Cancer letters · 2025Review
- The solid tumor microenvironment and related targeting strategies: a concise review.Frontiers in immunology · 2025Review
- Characterization of Gold-Enhanced Titania: Boosting Cell Proliferation and Combating Bacterial Infestation.Tissue engineering and regenerative medicine · 2024Article
- Prospect of Gold Nanoparticles in Pancreatic Cancer.Pharmaceutics · 2024Review
- Antibody and siRNA Nanocarriers to Suppress Wnt Signaling, Tumor Growth, and Lung Metastasis in Triple-Negative Breast Cancer.Advanced therapeutics · 2024Article
- Biodistribution and therapeutic efficacy of a gold nanoparticle-based targeted drug delivery system against pancreatic cancer.Cancer letters · 2024Article
- Nanoparticles in tumor microenvironment remodeling and cancer immunotherapy.Journal of hematology & oncology · 2024Review
- Remodeling the tumor-immune microenvironment by anti-CTLA4 blockade enhanced subsequent anti-PD-1 efficacy in advanced nasopharyngeal carcinoma.NPJ precision oncology · 2024Article
- Metal nanoparticles as a potential technique for the diagnosis and treatment of gastrointestinal cancer: a comprehensive review.Cancer cell international · 2023Review
- Review
- Gold nanoparticles combat enveloped RNA virus by affecting organelle dynamics.Signal transduction and targeted therapy · 2023Article
- Chronic Inflammation's Transformation to Cancer: A Nanotherapeutic Paradigm.Molecules (Basel, Switzerland) · 2023Review
- Article
- Molecular and cellular effects of gold nanoparticles treatment in experimental diabetic myopathy.Heliyon · 2022Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Altered tumor microenvironment (TME) arising from a bidirectional crosstalk between the pancreatic cancer cells (PCCs) and the pancreatic stellate cells (PSCs) is implicated in the dismal prognosis in pancreatic ductal adenocarcinoma (PDAC), yet effective strategies to disrupt the crosstalk is lacking. Here, we demonstrate that gold nanoparticles (AuNPs) inhibit proliferation and migration of both PCCs and PSCs by disrupting the bidirectional communication via alteration of the cell secretome. Analyzing the key proteins identified from a functional network of AuNP-altered secretome in PCCs and PSCs, we demonstrate that AuNPs impair secretions of major hub node proteins in both cell types and transform activated PSCs toward a lipid-rich quiescent phenotype. By reducing activation of PSCs, AuNPs inhibit matrix deposition, enhance angiogenesis, and inhibit tumor growth in an orthotopic co-implantation model in vivo. Auto- and heteroregulations of secretory growth factors/cytokines are disrupted by AuNPs resulting in reprogramming of the TME. By utilizing a kinase dead mutant of IRE1-α, we demonstrate that AuNPs alter the cellular secretome through the ER-stress-regulated IRE1-dependent decay pathway (RIDD) and identify endostatin and matrix metalloproteinase 9 as putative RIDD targets. Thus, AuNPs could potentially be utilized as a tool to effectively interrogate bidirectional communications in the tumor microenvironment, reprogram it, and inhibit tumor growth by its therapeutic function.
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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 OpenQuestion graph.