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Endothelial-monocyte-activating polypeptide II induces rat C6 glioma cell apoptosis via the mitochondrial pathway

Li-Bo Liu1, Hui Xie1, Yi-Xue Xue1

  • 1Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110001, PR China; Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110001, PR China.

Biochemical and Biophysical Research Communications
|January 21, 2015
PubMed

Insights

Endothelial-monocyte-activating polypeptide II (EMAP II) effectively inhibits rat glioma C6 cell growth by triggering apoptosis. This process involves the mitochondrial pathway, reactive oxygen species (ROS), and the Bax/Bcl-2 protein ratio.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Gliomas are primary brain tumors with limited treatment options.
  • Identifying novel therapeutic agents to induce cancer cell apoptosis is crucial.

Purpose of the Study:

  • To investigate the anti-glioma effects of Endothelial-monocyte-activating polypeptide II (EMAP II).
  • To determine if EMAP II induces apoptosis in rat brain glioma C6 cells.
  • To elucidate the molecular mechanisms underlying EMAP II-induced apoptosis.

Main Methods:

  • Cell viability assays were performed on rat C6 glioma cells treated with EMAP II.
  • Apoptosis was assessed by measuring changes in mitochondrial membrane potential and cytochrome c release.
  • Caspase activation, reactive oxygen species (ROS) production, and expression levels of Bax, Apaf-1, and Bcl-2 were analyzed.

Main Results:

  • EMAP II significantly reduced C6 glioma cell viability in a time-dependent manner.
  • EMAP II treatment led to increased apoptosis, decreased mitochondrial membrane potential, and cytochrome c release.
  • EMAP II induced ROS generation and altered the expression of apoptosis-related proteins (Bax, Apaf-1, Bcl-2).

Conclusions:

  • EMAP II effectively inhibits glioma C6 cell growth by inducing apoptosis.
  • The mitochondrial pathway, involving caspase activation and ROS production, mediates EMAP II-induced apoptosis.
  • The Bax/Bcl-2 ratio plays a role in the apoptotic process triggered by EMAP II.
Keywords:
ApoptosisBaxBcl-2EMAP IIGliomaReactive oxygen species

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