BCL2L13 promotes mitophagy through DNM1L-mediated mitochondrial fission in glioblastoma

Jiwei Wang1,2, Anbin Chen3, Zhiwei Xue1,2

  • 1Department of Neurosurgery, Qilu Hospital, Cheeloo College of Medicine and Institute of Brain and Brain-Inspired Science, Shandong University, 250012, Jinan, China.

Cell Death & Disease
|September 2, 2023
PubMed

Insights

Bcl2-like 13 (BCL2L13) promotes Glioblastoma multiforme (GBM) growth by increasing mitochondrial fission and mitophagy. Targeting BCL2L13 offers a potential therapeutic strategy for GBM patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Glioblastoma multiforme (GBM) requires new diagnostic and therapeutic approaches.
  • BCL2 like 13 (BCL2L13), a BCL2 family member, influences tumor cell growth and apoptosis.
  • The role and mechanism of BCL2L13 in GBM are not well understood.

Purpose of the Study:

  • To investigate the clinical significance, biological role, and mechanism of BCL2L13 in Glioblastoma multiforme.
  • To determine if BCL2L13 expression is altered in GBM and its functional impact.

Main Methods:

  • Analysis of BCL2L13 expression in GBM cell lines and clinical tissues.
  • Investigation of the molecular mechanism involving BCL2L13, DNM1L, mitochondrial fission, and mitophagy.
  • Assessment of the functional role of BCL2L13 in GBM cell proliferation and invasion in vitro and in vivo.

Main Results:

  • BCL2L13 expression was significantly upregulated in GBM cell lines and patient samples.
  • BCL2L13 was found to target DNM1L at Ser616, inducing mitochondrial fission and increased mitophagy.
  • Upregulation of BCL2L13 promoted GBM cell proliferation and invasion.

Conclusions:

  • BCL2L13 promotes GBM progression through DNM1L-mediated mitochondrial fission and enhanced mitophagy.
  • BCL2L13 represents a potential molecular target for novel GBM therapies.

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