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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Sevoflurane: A dual modulator of miR‑211‑5p and mitochondrial apoptosis in glioma therapy.

Haili Wang1, Guofang Cheng2, Shuyuan Zhang1

  • 1Department of Anesthesiology, Sanmenxia Central Hospital of Henan University of Science and Technology, Sanmenxia, Henan 472000, P.R. China.

Molecular Medicine Reports
|April 25, 2025
PubMed
Summary

Sevoflurane (SEV) triggers glioma cell apoptosis via the mitochondrial pathway by upregulating microRNA-211-5p (miR-211-5p). This process involves regulating SIRT1 and inhibiting the PI3K/AKT pathway, offering potential glioma treatment avenues.

Keywords:
cancer therapygliomamicroRNA‑211‑5pmitochondria‑dependent apoptosisprotein kinase pathwaysevofluranesilent information regulator 1

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Oncology

Background:

  • Glioma is a primary brain tumor with limited treatment options.
  • Understanding the molecular mechanisms of apoptosis induction is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of sevoflurane (SEV) in regulating glioma cell apoptosis.
  • To elucidate the involvement of the mitochondrial apoptosis pathway, microRNA-211-5p (miR-211-5p), SIRT1, and the PI3K/AKT signaling pathway in SEV-induced apoptosis.

Main Methods:

  • Cell viability, apoptosis, and mitochondrial function assays were performed.
  • Expression levels of miR-211-5p, SIRT1, and PI3K/AKT pathway proteins were analyzed using RT-qPCR and Western blotting.
  • Dual luciferase reporter gene assay confirmed the interaction between miR-211-5p and SIRT1.

Main Results:

  • Sevoflurane suppressed glioma cell proliferation and induced apoptosis via the mitochondrial pathway.
  • SEV treatment increased miR-211-5p levels in glioma cells.
  • SEV upregulated miR-211-5p, which downregulated SIRT1 and inhibited the PI3K/AKT pathway, leading to apoptosis.

Conclusions:

  • Sevoflurane promotes glioma cell apoptosis by upregulating miR-211-5p, which targets SIRT1 and modulates the SIRT1/PI3K/AKT signaling pathway.
  • This mechanism mediates mitochondria-dependent apoptosis, suggesting SEV as a potential therapeutic agent for glioma.