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Published on: July 29, 2011
FERMT1 suppression induces anti-tumor effects and reduces stemness in glioma cancer cells
Zhigang Pan1, Chuhan Ke1, Hanlin Zheng1
1Department of Neurosurgery, The Second Affiliated Hospital, Fujian Medical University, 34# zhongshan North Road, Quanzhou, Fujian, 362000, China.
Objective:
Glioma is a leading cause of mortality worldwide, its recurrence poses a major challenge in achieving effective treatment outcomes. Cancer stem cells (CSCs) have emerged as key contributors to tumor relapse and chemotherapy resistance, making them attractive targets for glioma cancer therapy. This study investigated the potential of FERMT1 as a prognostic biomarker and its role in regulating stemness through cell cycle in glioma.
Methods:
Using data from TCGA-GBM, GSE4290, GSE50161 and GSE147352 for analysis of FERMT1 expression in glioma tissues. Then, the effects of FERMT1 knockdown on cell cycle, proliferation, sphere formation ability, invasion and migration were investigated. The influences of FERMT1 on expression of glycolysis-related proteins and levels of ATP, glucose, lactate and G6PDH were also explored. Furthermore, the effects of FERMT1 knockdown on cellular metabolism were evidenced.
Results:
Significant upregulation of FERMT1 in glioma tissues was observed. Silencing FERMT1 not only affected the cell cycle but also led to a notable reduction in proliferation, invasion and migration. The expression of glycolysis-associated proteins including GLUT1, GLUT3, GLUT4, and SCO2 were reduced by FERMT1 knockdown, resulted in increased ATP and glucose as well as decreased lactic acid and G6PDH levels. FERMT1 knockdown also inhibited cellular metabolism. Moreover, FERMT1 knockdown significantly reduced sphere diameter, along with inhibiting the expression of transcription factors associated with stemness in glioma cells.
Conclusion:
These findings demonstrated that FERMT1 could be an ideal target for the advancement of innovative strategies against glioma treatment via modulating cellular process involved in stemness regulation and metabolism.
Insights
FERMT1 is upregulated in glioma and drives cancer stem cell properties. Silencing FERMT1 inhibits glioma cell proliferation, migration, and metabolism, suggesting FERMT1 as a therapeutic target for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma recurrence and chemotherapy resistance are significant challenges in cancer treatment.
- Cancer stem cells (CSCs) are implicated in glioma relapse and resistance.
- Identifying novel biomarkers and therapeutic targets is crucial for improving glioma outcomes.
Purpose of the Study:
- To investigate the role of FERMT1 as a prognostic biomarker in glioma.
- To explore FERMT1's influence on cancer stemness regulation via the cell cycle.
- To assess FERMT1's impact on glioma cell metabolism and chemosensitivity.
Main Methods:
- Analysis of FERMT1 expression in glioma tissues using TCGA-GBM and GEO datasets (GSE4290, GSE50161, GSE147352).
- Functional assays including cell cycle analysis, proliferation, sphere formation, invasion, and migration assays after FERMT1 knockdown.
- Assessment of glycolysis-related protein expression, ATP, glucose, lactate, and G6PDH levels.
Main Results:
- FERMT1 expression is significantly upregulated in glioma tissues.
- FERMT1 knockdown reduced glioma cell proliferation, invasion, migration, and sphere formation.
- Silencing FERMT1 altered cell cycle progression and inhibited cellular metabolism, including glycolysis.
- FERMT1 knockdown decreased the expression of stemness-associated transcription factors.
Conclusions:
- FERMT1 plays a critical role in regulating glioma stemness and cellular metabolism.
- FERMT1 is a potential prognostic biomarker and therapeutic target for glioma.
- Targeting FERMT1 may offer innovative strategies to overcome glioma recurrence and chemoresistance.
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