4.7 Article

Momordica charantia-derived extracellular vesicles-like nanovesicles inhibited glioma proliferation, migration, and invasion by regulating the PI3K/AKT signaling pathway

期刊

JOURNAL OF FUNCTIONAL FOODS
卷 90, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.jff.2022.104968

关键词

Momordica.charantia-derived extracellular vesicles-like nanovesicles; Glioma therapy; Proliferation; Migration; Invasion

资金

  1. National Natural Science Foundation of China [81671164, 81802086]
  2. Natural Science Foundation of Jiangsu Province [BK20211348]
  3. Scientific Research Project of Jiangsu Provincial Healthy Commission [ZDB2020024]
  4. Xuzhou Basic Research Project [KC21030]
  5. Postgraduate Research & Practice Innovation Program of JiangsuProvince [KYCX20_2502, KYCX21_2722]
  6. Specialized Research Fund for Senior Personnel Program [D2019028]
  7. Young Science and Technology Innovation Team of Xuzhou Medical University [TD202005]

向作者/读者索取更多资源

Momordica.charantia-derived extracellular vesicles-like nanovesicles (MCELNs) have the potential to treat glioma by inhibiting cell proliferation and migration, and may be associated with the PI3K/AKT pathway.
Momordica.charantia has antioxidant and neuroprotective effects, but its anti-glioma capacity remains unclear. Plant-derived nanovesicles have shown therapeutic potential in inflammation and cancer. This study explored the therapeutic effects of Momordica.charantia-derived extracellular vesicles-like nanovesicles (MCELNs) in treating glioma and its underlying mechanisms. The MCELNs were successfully isolated and characterized similarly to animal cell-derived extracellular vesicles. The in vitro assays identified that MCELNs inhibited the proliferation but did not promote apoptosis of U251 glioma cells. MCELNs repressed U251 glioma cells migration and invasion via proceeding the epithelial-mesenchymal transition process and downregulating MMP9. MCELNs penetrated the BBB and suppressed the glioma growth and metastasis in vivo. The ratios of p-AKT/AKT and pPI3K/PI3K were downregulated in MCELNs treated U251 glioma cells compared with the control. Highly expressed miR5813 in MCELNs might be involved in the PI3K/AKT pathway that needs further investigation. MCELNs could serve as a novel therapeutic strategy for glioma treatment.

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