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Over-expression of tetraspanin 8 in malignant glioma regulates tumor cell progression
Si-Jian Pan1, Yue-Bing Wu2, Shang Cai3
1Department of Neurosurgery, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China.
Abstract:
Tumor cell invasion and proliferation remain the overwhelming causes of death for malignant glioma patients. To establish effective therapeutic methods, new targets implied in these processes have to be identified. Tetraspanin 8 (Tspn8) forms complexes with a large variety of trans-membrane and/or cytosolic proteins to regulate several important cellular functions. In the current study, we found that Tspn8 was over-expressed in multiple clinical malignant glioma tissues, and its expression level correlated with the grade of tumors. Tspn8 expression in malignant glioma cells (U251MG and U87MG lines) is important for cell proliferation and migration. siRNA-mediated knockdown of Tspn8 markedly reduced in vitro proliferation and migration of U251MG and U87MG cells. Meanwhile, Tspn8 silencing also increased the sensitivity of temozolomide (TMZ), and significantly increased U251MG or U87MG cell death and apoptosis by TMZ were achieved with Tspn8 knockdown. We observed that Tspn8 formed a complex with activated focal adhesion kinase (FAK) in both human malignant glioma tissues and in above glioma cells. This complexation appeared required for FAK activation, since Tspn8 knockdown inhibited FAK activation in U251MG and U87MG cells. These results provide evidence that Tspn8 contributes to the pathogenesis of glioblastoma probably by promoting proliferation, migration and TMZ-resistance of glioma cells. Therefore, targeting Tspn8 may provide a potential therapeutic intervention for malignant glioma.
Insights
Tetraspanin 8 (Tspn8) promotes malignant glioma growth and resistance to temozolomide (TMZ). Targeting Tspn8 may offer a new therapeutic strategy for glioblastoma by inhibiting proliferation and migration.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Malignant glioma is a deadly cancer where tumor cell invasion and proliferation are primary causes of death.
- Identifying novel therapeutic targets is crucial for developing effective treatments for malignant glioma.
- Tetraspanin 8 (Tspn8) is a transmembrane protein involved in regulating cellular functions.
Purpose of the Study:
- To investigate the role of Tetraspanin 8 (Tspn8) in malignant glioma.
- To determine if Tspn8 expression correlates with tumor grade and affects glioma cell proliferation, migration, and response to temozolomide (TMZ).
- To explore the interaction between Tspn8 and focal adhesion kinase (FAK) in glioma.
Main Methods:
- Analysis of Tspn8 expression in clinical malignant glioma tissues and cell lines (U251MG, U87MG).
- siRNA-mediated knockdown of Tspn8 to assess its impact on cell proliferation, migration, and apoptosis.
- Investigation of the Tspn8-FAK complex formation and its effect on FAK activation.
- Assessment of Tspn8 knockdown's influence on temozolomide (TMZ) sensitivity.
Main Results:
- Tspn8 was over-expressed in malignant glioma tissues, with expression levels correlating with tumor grade.
- Tspn8 knockdown significantly reduced proliferation and migration of U251MG and U87MG cells.
- Silencing Tspn8 enhanced sensitivity to temozolomide (TMZ), leading to increased cell death and apoptosis.
- Tspn8 formed a complex with activated focal adhesion kinase (FAK), and Tspn8 knockdown inhibited FAK activation.
Conclusions:
- Tspn8 promotes glioblastoma pathogenesis by enhancing proliferation, migration, and temozolomide (TMZ) resistance.
- Tspn8's role in FAK activation is critical for its function in glioma cells.
- Targeting Tspn8 presents a potential therapeutic strategy for malignant glioma.
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