INHBB promotes tumor aggressiveness and stemness of glioblastoma via activating EGFR signaling

Background: As most common primary tumor in adult's brain, the glioblastoma (GBM) still ends up with poor survival period. Little progress has been made in recent decades in terms of improving prognosis. There's still an urgent need for novel targets and strategies to overcome such malignancy. Methods: Both the Cancer Genome Atlas and Gene Expression Omnibus databases were used to analyze expression differences and correlations. The immunohistochemistry and survival analysis were used to verify expression differences. Tumorigenesis was assessed using cholecystokinin and the orthotopic xenograft model. Metastasis was determined by the transwell assay and the tail vein xenograft model. Results: Inhibin subunit beta B (INHBB) was upregulated in GBM and predicted poor survival. It promoted tumor growth, invasion and stemness in GBM. INHBB expression correlated with the epidermal growth factor receptor (EGFR) expression and downstream AKT and ERK expression levels. The increased tumor progression induced by INHBB could be inhibited by afatinib. Conclusion: This study revealed INHBB as a tumor progression and independent prognostic factor in GBM, which could be a potential upper stream molecular of EGFR/ERK/AKT signaling.

Automated summary

This study identified INHBB as an upregulated gene in GBM that predicts poor prognosis. INHBB promotes tumor growth, invasion, and stemness in GBM and is correlated with the expression levels of EGFR and downstream AKT and ERK. The tumor progression induced by INHBB can be inhibited by afatinib.