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Published on: April 7, 2017
Targeting SIM2-s decreases glioma cell invasion through mesenchymal--epithelial transition
Yuhang Su1, Juntao Wang, Xiaodan Zhang
1Department of Emergency, Qi Lu Hospital, Shandong University, 250012, Jinan, China; Department of Neurosurgery, Qi Lu Hospital, Shandong University, 250012, Jinan, China.
Abstract:
Glioma is a common primary intracranial carcinoma with high incidence, recurrence, and motility. Single minded homolog 2-short form (SIM2-s), a member of basic helix-loop-helix (bHLH) family, is reported to be expressed in glioma and might play a role in the invasion. In the present study, we investigated the importance of SIM2-s in glioma invasion and further explored the potential mechanisms. We showed that targeting SIM2-s by interference technology could decrease cell adhesion to fibronectin, induce cell aggregation and cytoskeletal changes. Furthermore, we showed that targeting SIM2-s increased the expression of epithelial markers and decreased the expression of mesenchymal markers, that is mesenchymal-epithelial transition (MET). Targeting SIM2-s decreased self-renewal of glioma stem cells by tumor sphere formation assay. Taken together, our results indicated that MET is involved in the inhibition of glioma invasion by targeting SIM2-s, and SIM2-s may be a new gene target.
Insights
Targeting Single minded homolog 2-short form (SIM2-s) inhibits glioma invasion by promoting mesenchymal-epithelial transition (MET). This study identifies SIM2-s as a potential therapeutic target for reducing glioma cell motility and self-renewal.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cell Biology
Background:
- Glioma is a prevalent primary brain tumor characterized by high rates of recurrence and invasion.
- Single minded homolog 2-short form (SIM2-s), a basic helix-loop-helix (bHLH) family member, is implicated in glioma progression.
- The precise role of SIM2-s in glioma invasion requires further elucidation.
Purpose of the Study:
- To investigate the role of SIM2-s in glioma invasion.
- To explore the underlying molecular mechanisms, including mesenchymal-epithelial transition (MET).
- To assess the impact of targeting SIM2-s on glioma stem cell self-renewal.
Main Methods:
- Utilized interference technology to target SIM2-s expression in glioma cells.
- Analyzed changes in cell adhesion, aggregation, and cytoskeletal organization.
- Assessed the expression of epithelial and mesenchymal markers to evaluate MET.
- Employed tumor sphere formation assays to determine the effect on glioma stem cell self-renewal.
Main Results:
- Targeting SIM2-s significantly reduced glioma cell adhesion to fibronectin.
- SIM2-s inhibition induced cell aggregation and altered cytoskeletal dynamics.
- Interference with SIM2-s promoted mesenchymal-epithelial transition (MET), indicated by increased epithelial markers and decreased mesenchymal markers.
- Reduced self-renewal capacity of glioma stem cells was observed upon SIM2-s targeting.
Conclusions:
- SIM2-s plays a crucial role in promoting glioma invasion.
- Mesenchymal-epithelial transition (MET) is a key mechanism through which SIM2-s inhibition suppresses glioma invasion.
- SIM2-s represents a promising novel therapeutic target for glioma treatment.
