Unrevealing the dual role of paired box and sex determining region Y related high mobility group box in glioblastoma
Abstrak
Abstract This narrative review summarises glioblastoma (GBM), a very frequent invasive kind of brain tumour in the elderly that is extremely aggressive, resistant to treatment, and has a bad prognosis because of its substantial genetic and cellular heterogeneity. With a median survival of about 15 months, GBM is still an incurable cancer. This review takes full 3 months for collect all relevant knowledge about PAX and SOX gene families, which have crucial roles in the biology of GBM, as shown by recent developments in molecular pathology. Depending on certain gene expression patterns, members of these transcription factor families have been shown to have both oncogenic and tumor suppressive properties. They are important regulators of brain development, stem cell maintenance, and tumor progression. While PAX6 functions as a tumor suppressor, preventing growth and angiogenesis, PAX3, PAX5, and PAX8 are increased in GBM, encouraging proliferation, stemness, and survival. Similarly, SOX7 and SOX11 act as suppressors, and their downregulation is associated with malignancy and a bad prognosis, while SOX2, SOX3, SOX4, and SOX9 increase tumor aggressiveness and resistance to treatment. Glioma cell migration, growth, and death inhibition are further fueled through the complex interactions between canonical and non-canonical WNT signaling that modulate PAX and SOX pathways. These results highlight how crucial thorough molecular profiling is for improved categorization, prognostication, and the creation of focused treatment plans in GBM. The discovery of the dual functions of the PAX and SOX genes in GBM highlights their potential as therapeutic targets and biomarkers, opening up new possibilities for more individualised and accurate treatment approaches.
Topik & Kata Kunci
Penulis (2)
Kallol Polley
Sayed Mohammed Firdous
Akses Cepat
- Tahun Terbit
- 2026
- Sumber Database
- DOAJ
- DOI
- 10.1007/s12672-026-04671-4
- Akses
- Open Access ✓