ITPKA suppresses glioma progression and predicts patient prognosis
Background: Inositol 1,4,5-trisphosphate 3-kinase A (ITPKA) is expressed in various tumors and is associated with tumor progression. This study investigated the expression patterns of ITPKA in gliomas and explored its functional role in glioblastoma (GBM), thereby providing new insights into the diagnostic and prognostic evaluations of ITPKA in this disease. Methods: ITPKA expression levels in glioma tissues of different World Health Organization (WHO) grades and GBM cell lines were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting. U251-MG and T98G cells were transfected with negative control, ITPKA overexpression or ITPKA knockdown plasmids, followed by relevant detections. Subsequently, the viability, proliferation, migration and invasion abilities, cell cycle progression, and apoptosis rate of GBM cells in each group were detected using the Cell-Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) proliferation, wound healing, Transwell, and flow cytometry assays, respectively. Subsequently, the effect of ITPKA on GBM growth was evaluated in a nude mouse subcutaneous tumor xenograft model. Results: and the progression of subcutaneous xenograft tumors in these two GBM cell lines in nude mice. Conclusions: Low expression of ITPKA in glioma tissues correlates with GBM progression, indicating that it may act as a tumor suppressor gene and is a candidate biomarker for the molecular diagnostic and prognostic evaluations of glioblastoma.
Authors
- Shizhang Ling (ORCID: https://orcid.org/0000-0002-6856-3577)
- Jun Liu
- Naiyue Zhang
- Min Peng
Institutions
- Wannan Medical College (CN)
- Hainan Medical College Hospital (CN)
- First Affiliated Hospital of Wannan Medical College (CN)
Publication Details
- Journal
- Frontiers in Oncology
- Published
- 2026-04-22
- DOI
- https://doi.org/10.3389/fonc.2026.1802857
- Primary Topic
- FOXO transcription factor regulation
- Type
- article
- Field-Weighted Citation Impact
- 0.00