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

in Artificial cells, nanomedicine, and biotechnology by Gang Wang, Jun-Jie Wang, Yu-Zhu Wang, Shi Feng, Gao Jing, Xing-Li Fu

TLDR

  • The study demonstrates the efficacy of myricetin nanoliposomes in inhibiting GBM cell proliferation and regulating proteins involved in glycolytic metabolism and cell survival.

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.

Overview

  • The study investigated the efficacy of myricetin incorporated nanoliposomes in treating glioblastoma multiforme (GBM) by inhibiting cell proliferation and regulating proteins related to glycolytic metabolism and cell survival.
  • The study used the GBM cell line DBTRG-05MG and employed nanoliposomes to deliver myricetin, a flavonoid with potential anti-tumor properties.
  • The primary objective of the study was to explore the prospect of myricetin nanoliposomes as an adjuvant therapy in glioblastoma treatment by targeting alternative cell death pathways.

Comparative Analysis & Findings

  • The myricetin nanoliposomes (MYR-NLs) demonstrated potent inhibition of proliferation in GBM cells and significantly regulated the levels of proteins related to glycolytic metabolism and cell survival.
  • MYR-NLs also down-regulated SIRT3 and phosphorylated p53, indicating that they inhibited GBM cell growth through the SIRT3/p53-mediated PI3K/Akt-ERK and mitochondrial pathways.
  • The study's findings provide rational evidence that liposomal myricetin targeted at alternative cell death pathways may be a useful adjuvant therapy in glioblastoma treatment.

Implications and Future Directions

  • The study's findings suggest that myricetin nanoliposomes may be a potential adjuvant therapy in glioblastoma treatment, offering a new approach for targeting alternative cell death pathways.
  • Future studies should investigate the in vivo efficacy of myricetin nanoliposomes in GBM treatment and explore their potential combination with existing therapies.
  • Additionally, the study highlights the importance of understanding the mechanisms of action of myricetin nanoliposomes in GBM cells, which may lead to the development of new therapeutic strategies.
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