The anti-cancer role of tumor protein p53-inducible nuclear protein 2/nuclear factor-kB/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway in spinal cord glioma.

OBJECTIVE

The function of tumor protein p53-inducible nuclear protein 2 (TP53INP2) in numerous cancers has been elucidated, but its role across the development of spinal cord glioma (SCG) remains largely unexplored. This study aims to explore the anti-cancer effect of TP53INP2/nuclear factor-kappa B (NF-kB)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway in SCG.

MATERIAL AND

METHODS

Quantitative real-time polymerase chain reaction was employed to determine TP53INP2 messenger RNA expression in vitro. Western blot analysis was conducted to detect TP53INP2, epithelial-tomesenchymal transition (EMT) marker, and NF-kB/Nrf2/HO-1 pathway protein. The proliferative potentials of glioma cells were assessed by 5-ethynyl-2'-deoxyuridine, colony formation, and cell counting kit-8 assays. Transwell assays were used to evaluate migratory and invasive capacities. Apoptotic cells and reactive oxygen species were analyzed using flow cytometer. Enzyme-linked immunosorbent assay was performed to measure superoxide dismutase and glutathione peroxidase levels. A tumor xenograft model in mouse was established.

RESULTS

High expression of TP53INP2 was observed in glioma cells. TP53INP2 depletion significantly inhibited tumor growth, metastasis, EMT, and oxidative stress and increased the apoptosis rate and number of immune cells. The silenced TP53INP2 hampered the activation of NF-kB and promoted the activation of the Nrf2/HO-1 pathway.

CONCLUSION

This work highlights the therapeutic potential of TP53INP2/NF-kB/Nrf2/HO-1 axis in SCG.