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Published on: November 30, 2022
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.
Abstract:
There is an urgent need for novel diagnostic and therapeutic strategies for patients with Glioblastoma multiforme (GBM). Previous studies have shown that BCL2 like 13 (BCL2L13) is a member of the BCL2 family regulating cell growth and apoptosis in different types of tumors. However, the clinical significance, biological role, and potential mechanism in GBM remain unexplored. In this study, we showed that BCL2L13 expression is significantly upregulated in GBM cell lines and clinical GBM tissue samples. Mechanistically, BCL2L13 targeted DNM1L at the Ser616 site, leading to mitochondrial fission and high mitophagy flux. Functionally, these alterations significantly promoted the proliferation and invasion of GBM cells both in vitro and in vivo. Overall, our findings demonstrated that BCL2L13 plays a significant role in promoting mitophagy via DNM1L-mediated mitochondrial fission in GBM. Therefore, the regulation and biological function of BCL2L13 render it a candidate molecular target for treating GBM.
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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