Background: Niban-like protein 2 (NIBAN2) has recently been linked to various neurological diseases; however, its exact role in glioma development remains unclear.
Methods: Quantitative reverse transcription-polymerase chain reaction, western blotting, and immunohistochemistry were used to evaluate NIBAN2 expression in glioma tissues. In addition, we examined the effects of NIBAN2 on glioma progression in various functional trials. Animal models were used to clarify the role of NIBAN2, especially its impact on the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway.
Results: The research outcomes revealed that NIBAN2 was highly upregulated in gliomas and its levels were strongly correlated with tumor grade and clinical outcomes. Functional assays showed that NIBAN2 enhanced glioma cell aggressiveness by activating JAK2/STAT3 signaling and promoted tumor growth by preventing apoptosis and accelerating the cell cycle.
Conclusion: The findings of this study show that NIBAN2 plays a key role in glioma aggression and poor prognosis, suggesting that it is a potential therapeutic target.
Keywords: JAK2/STAT3/MYC; NIBAN2; gliomas; proliferation.
© 2025 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd.