High PGC-1α Expression as a Poor Prognostic Indicator in Intracranial Glioma

Author:

Cheng Yu-Wen12ORCID,Lee Jia-Hau3,Chang Chih-Hui4,Tseng Tzu-Ting4,Chai Chee-Yin256,Lieu Ann-Shung47,Kwan Aij-Lie2478

Affiliation:

1. Department of Neurosurgery, Kaohsiung Veterans General Hospital, Kaohsiung 807, Taiwan

2. Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

3. National Institute of Cancer Research, National Health Research Institutes, Tainan 701, Taiwan

4. Division of Neurosurgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan

5. Department of Pathology, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan

6. Department of Pathology, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

7. Department of Surgery, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan

8. Department of Neurosurgery, University of Virginia, Charlottesville, VA 23806, USA

Abstract

Gliomas are the most common primary brain tumors in adults. Despite multidisciplinary treatment approaches, the survival rates for patients with malignant glioma have only improved marginally, and few prognostic biomarkers have been identified. Peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α) is a crucial regulator of cancer metabolism, playing a vital role in cancer cell adaptation to fluctuating energy demands. In this study, the clinicopathological roles of PGC-1α in gliomas were evaluated. Employing immunohistochemistry, cell culture, siRNA transfection, cell viability assays, western blot analyses, and in vitro and in vivo invasion and migration assays, we explored the functions of PGC-1α in glioma progression. High PGC-1α expression was significantly associated with an advanced pathological stage in patients with glioma and with poorer overall survival. The downregulation of PGC-1α inhibited glioma cell proliferation, invasion, and migration and altered the expression of oncogenic markers. These results conclusively demonstrated that PGC-1α plays a critical role in maintaining the malignant phenotype of glioma cells and indicated that targeting PGC-1α could be an effective strategy to curb glioma progression and improve patient survival outcomes.

Funder

Kaohsiung Medical University Chung-Ho Memorial Hospital

Publisher

MDPI AG

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