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HMSN-Mediated miR-502-3p Delivery Suppresses Lung Adenocarcinoma via TPX2-Dependent Inhibition of PI3K/AKT
Mingzheng Jiang1,2, Yangyuyan Bai1,2, Jiwei Li3
1Department of Respiratory, Critical Care and Sleep Medicine, Xiang' An Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361101, China.
Abstract:
Lung adenocarcinoma (LUAD) is a prevalent subtype of nonsmall cell lung cancer with high mortality, underscoring the need for novel therapeutic strategies. Here, we demonstrated that the intravenous delivery of miR-502-3p via hollow mesoporous silica nanoparticles (HMSN; miR@HM-NH2) dramatically suppresses LUAD xenograft growth with negligible toxicity. MiR-502-3p is significantly downregulated in LUAD tissues and correlates with poor differentiation, metastasis, advanced TNM stage, and reduced overall survival, as shown by clinical samples and TCGA analysis. In vitro, miR-502-3p overexpression inhibited proliferation, migration, and invasion in LUAD cell lines, including PC9 and H1975 cells. Mechanistically, dual-luciferase assays and RNA-seq identified TPX2 as a direct target of miR-502-3p. miR-502-3p-mediated TPX2 inhibition downregulated phosphorylation of PI3K and AKT, with no reciprocal regulation on TPX2. Collectively, our findings reveal that the miR-502-3p/TPX2/PI3K/AKT axis plays a critical tumor-suppressive role in LUAD, with HMSN-based miR-502-3p delivery offering a promising therapeutic strategy.
Insights
Intravenous delivery of microRNA-502-3p (miR-502-3p) using hollow mesoporous silica nanoparticles effectively suppresses lung adenocarcinoma growth. This novel therapeutic strategy shows promise for treating this aggressive cancer with minimal toxicity.
Area of Science:
- Oncology
- Molecular Biology
- Nanomedicine
Background:
- Lung adenocarcinoma (LUAD) presents a significant global health challenge due to high mortality rates.
- There is an urgent need for innovative therapeutic approaches to combat LUAD progression and improve patient outcomes.
Purpose of the Study:
- To investigate the therapeutic potential of miR-502-3p delivered via hollow mesoporous silica nanoparticles (HMSN) for lung adenocarcinoma.
- To elucidate the molecular mechanisms underlying miR-502-3p's tumor-suppressive function in LUAD.
Main Methods:
- Intravenous administration of miR-502-3p loaded HMSN (miR@HM-NH2) in LUAD xenograft models.
- Analysis of miR-502-3p expression in clinical LUAD tissues and The Cancer Genome Atlas (TCGA) database.
- In vitro studies using LUAD cell lines (PC9, H1975) to assess proliferation, migration, and invasion.
- Dual-luciferase reporter assays and RNA sequencing to identify direct molecular targets and downstream signaling pathways.
Main Results:
- miR-502-3p was significantly downregulated in LUAD tissues, correlating with advanced disease and poor survival.
- miR@HM-NH2 treatment suppressed LUAD xenograft growth with negligible toxicity.
- Overexpression of miR-502-3p inhibited LUAD cell proliferation, migration, and invasion in vitro.
- TPX2 was identified as a direct target of miR-502-3p, and its inhibition downregulated PI3K/AKT phosphorylation.
Conclusions:
- The miR-502-3p/TPX2/PI3K/AKT signaling axis plays a crucial tumor-suppressive role in lung adenocarcinoma.
- HMSN-mediated delivery of miR-502-3p represents a potent and safe therapeutic strategy for LUAD.
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