ArticleiScience2026
Hyaluronic acid and folic acid-modified mesoporous silica nanoparticles delivering sulforaphane suppress NSCLC via SPI1/miR-616-5p axis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
Sulforaphane (SF) suppresses NSCLC metastasis by modulating miR-616-5p, which is transcriptionally upregulated by the oncogenic transcription factor SPI1. However, the roles of SF, SPI1, and miR-616-5p in NSCLC metastasis remain unclear. In this study, we found that SPI1 expression in NSCLC tissues positively correlated with miR-616-5p levels, and that SPI1 transcriptionally regulated miR-616-5p to promote NSCLC cell invasion and migration. Further analysis showed that SF directly binds SPI1, inhibiting its activity and downregulating miR-616-5p expression, thereby attenuating NSCLC metastasis. However, the poor stability of SF limits its clinical application. To address this, we developed a mesoporous silica nanoparticle (MSN)-based delivery system modified with hyaluronic acid and folic acid (MSNs@SF-HA-FA), which exhibited good stability, enhanced cellular uptake, and improved tumor targeting and anti-metastatic efficacy in NSCLC xenograft models. Collectively, our findings reveal the SPI1/miR-616-5p axis drives NSCLC metastasis and show that MSNs@SF-HA-FA enhances SF's anti-metastatic effect, highlighting its clinical potential.
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