Se@SiO2@mSiO2 nanoparticle inhibits cellular oxidative stress and Wnt/β-catenin pathway by inhibiting AGGF1 expression in the treatment of prostate cancer
7 affiliations
- 1Department of Urology, Capital Medical University Beijing Friendship Hospital, Beijing, China.
- 2Institute of Urology, Beijing Municipal Health Commission, Beijing, China.
- 3Department of Urology, Beijing Electric Power Hospital of State Grid Corporation of China, Beijing, China.
- 4Department of Immunology, School of Cell and Gene Therapy, Songjiang Research Institute, Shanghai Jiaotong University School of Medicine Affiliated Songjiang Hospital, Shanghai, China.
- 5College of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai, China.
- 6Precision Research Center for Refractory Diseases, Institute for Clinical Research, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
- 7Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Abstract
Background and objective
Advances in nanomedicine have introduced promising strategies for enhancing drug bioavailability, tumor targeting, and controlled release. This study aimed to investigate the regulatory role of angiogenic factor with G patch and FHA domains 1 (AGGF1) in prostate cancer progression and to evaluate the therapeutic potential of a double-layered silica-shelled selenium nanoparticle (Se@SiO₂@mSiO₂) targeting the AGGF1-associated signaling network.Methods
We performed bioinformatics analyses based on the TCGA-PRAD dataset, including differential expression analysis, WGCNA, and functional enrichment, to identify AGGF1-related pathways. Clinical specimens from 54 prostate cancer patients were collected for validation through Western Blot and immunohistochemistry. We synthesized Se@ SiO₂@mSiO₂ via a double-layer coating technique and characterized its physicochemical properties by TEM, XRD, XPS, and selenium release assays. To assess the anti-tumor effects of Se@SiO₂@mSiO₂, we employed CCK-8, colony formation assays, oxidative stress detection, and established both subcutaneous and orthotopic tumor models in BALB/c nude mice. We further conducted ChIP-qPCR and gene overexpression/silencing experiments to delineate the upstream-downstream relationship between AGGF1 and the Wnt/β-catenin pathway.Results
AGGF1 was significantly overexpressed in prostate cancer tissues compared with adjacent normal tissues, and high AGGF1 expression was associated with advanced tumor stage, higher Gleason score, and poorer disease-free and overall survival. Se@SiO₂@mSiO₂ exhibited a sustained selenium release profile and demonstrated effective intracellular uptake. Treatment with Se@SiO₂@mSiO₂ inhibited prostate cancer cell proliferation in a concentration-and time-dependent manner, reduced AGGF1 expression, suppressed oxidative damage, and downregulated β-catenin expression. Overexpression of AGGF1 partially reversed the anti-proliferative effects and Wnt/β-catenin pathway inhibition induced by Se@SiO₂@mSiO₂, whereas silencing β-catenin did not significantly alter AGGF1 expression, supporting the upstream regulatory position of AGGF1. In vivo experiments confirmed that Se@SiO₂@mSiO₂ significantly reduced tumor burden without detectable organ toxicity.Conclusion
AGGF1 functions as an upstream regulator connecting oxidative stress and Wnt/β-catenin signaling in prostate cancer. Se@SiO₂@mSiO₂ exerts anti-tumor effects by downregulating AGGF1 and subsequently suppressing both pathways. These findings position AGGF1 as a pivotal therapeutic target and validate Se@SiO₂@mSiO₂ as a candidate nanomedicine for precision treatment of prostate cancer.
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BibTeX
@article{lyu2026sesio2msio2,
title = {{Se@SiO2@mSiO2 nanoparticle inhibits cellular oxidative stress and Wnt/β-catenin pathway by inhibiting AGGF1 expression in the treatment of prostate cancer}},
author = {Jingcheng Lyu and Mingyu Chang and Lianhui Sun and Ruiyu Yue and Xijian Liu and Guangjian Fan and Aihong Chen and Wei Huang and Ye Tian and Boyu Yang},
journal = {Journal of translational internal medicine},
year = {2026},
month = oct,
doi = {10.1515/jtim-2026-0076},
url = {https://europepmc.org/article/PMC/PMC13726657},
note = {CC BY},
}
RIS
TY - JOUR
TI - Se@SiO2@mSiO2 nanoparticle inhibits cellular oxidative stress and Wnt/β-catenin pathway by inhibiting AGGF1 expression in the treatment of prostate cancer
AU - Jingcheng Lyu
AU - Mingyu Chang
AU - Lianhui Sun
AU - Ruiyu Yue
AU - Xijian Liu
AU - Guangjian Fan
AU - Aihong Chen
AU - Wei Huang
AU - Ye Tian
AU - Boyu Yang
PY - 2026
DA - 2026/10/23
JO - Journal of translational internal medicine
DO - 10.1515/jtim-2026-0076
UR - https://europepmc.org/article/PMC/PMC13726657
AB - Background and objective Advances in nanomedicine have introduced promising strategies for enhancing drug bioavailability, tumor targeting, and controlled release. This study aimed to investigate the regulatory role of angiogenic factor with G patch and FHA domains 1 (AGGF1) in prostate cancer progression and to evaluate the therapeutic potential of a double-layered silica-shelled selenium nanoparticle (Se@SiO₂@mSiO₂) targeting the AGGF1-associated signaling network.Methods We performed bioinformatics analyses based on the TCGA-PRAD dataset, including differential expression analysis, WGCNA, and functional enrichment, to identify AGGF1-related pathways. Clinical specimens from 54 prostate cancer patients were collected for validation through Western Blot and immunohistochemistry. We synthesized Se@ SiO₂@mSiO₂ via a double-layer coating technique and characterized its physicochemical properties by TEM, XRD, XPS, and selenium release assays. To assess the anti-tumor effects of Se@SiO₂@mSiO₂, we employed CCK-8, colony formation assays, oxidative stress detection, and established both subcutaneous and orthotopic tumor models in BALB/c nude mice. We further conducted ChIP-qPCR and gene overexpression/silencing experiments to delineate the upstream-downstream relationship between AGGF1 and the Wnt/β-catenin pathway.Results AGGF1 was significantly overexpressed in prostate cancer tissues compared with adjacent normal tissues, and high AGGF1 expression was associated with advanced tumor stage, higher Gleason score, and poorer disease-free and overall survival. Se@SiO₂@mSiO₂ exhibited a sustained selenium release profile and demonstrated effective intracellular uptake. Treatment with Se@SiO₂@mSiO₂ inhibited prostate cancer cell proliferation in a concentration-and time-dependent manner, reduced AGGF1 expression, suppressed oxidative damage, and downregulated β-catenin expression. Overexpression of AGGF1 partially reversed the anti-proliferative effects and Wnt/β-catenin pathway inhibition induced by Se@SiO₂@mSiO₂, whereas silencing β-catenin did not significantly alter AGGF1 expression, supporting the upstream regulatory position of AGGF1. In vivo experiments confirmed that Se@SiO₂@mSiO₂ significantly reduced tumor burden without detectable organ toxicity.Conclusion AGGF1 functions as an upstream regulator connecting oxidative stress and Wnt/β-catenin signaling in prostate cancer. Se@SiO₂@mSiO₂ exerts anti-tumor effects by downregulating AGGF1 and subsequently suppressing both pathways. These findings position AGGF1 as a pivotal therapeutic target and validate Se@SiO₂@mSiO₂ as a candidate nanomedicine for precision treatment of prostate cancer.
SN - 2450-131X
SN - 2224-4018
ER -