Myricetin nanoliposomes induced SIRT3-mediated glycolytic metabolism leading to glioblastoma cell death

Artif Cells Nanomed Biotechnol. 2018;46(sup3):S180-S191. doi: 10.1080/21691401.2018.1489825. Epub 2019 Jan 28.

Abstract

As the most aggressive and malignant glioma, glioblastoma multiforme (GBM) abnormally expresses genes that mediate glycolytic metabolism and tumour cell growth. In this study, we investigated myricetin incorporated nanoliposomes and ascertained their prospect in effectively treating cancer via the employment of the GBM cell line DBTRG-05MG. Notably, the myricetin nanoliposomes (MYR-NLs) displayed potent inhibition of proliferation and significantly regulated the levels of proteins related to both glycolytic metabolism and cell survival. Most importantly, SIRT3 and phosphorylated p53 were also down-regulated by MYR-NLs, indicating that the MYR-NLs inhibited GBM cell growth through the SIRT3/p53-mediated PI3K/Akt-ERK and mitochondrial pathways. Our findings thus provide rational evidence that liposomal myricetin targeted at alternative cell death pathways may be a useful adjuvant therapy in glioblastoma treatment.

Keywords: Glioblastoma; SIRT3; glycolytic metabolism; mitochondrial pathway; myricetin nanoliposomes.

MeSH terms

  • Apoptosis / drug effects*
  • Brain Neoplasms* / drug therapy
  • Brain Neoplasms* / metabolism
  • Brain Neoplasms* / pathology
  • Cell Line, Tumor
  • Flavonoids* / chemistry
  • Flavonoids* / pharmacology
  • Glioblastoma* / drug therapy
  • Glioblastoma* / metabolism
  • Glioblastoma* / pathology
  • Glycolysis / drug effects*
  • Humans
  • Liposomes
  • Nanoparticles* / chemistry
  • Nanoparticles* / therapeutic use
  • Neoplasm Proteins / biosynthesis*
  • Sirtuin 3 / biosynthesis*

Substances

  • Flavonoids
  • Liposomes
  • Neoplasm Proteins
  • myricetin
  • SIRT3 protein, human
  • Sirtuin 3