Background: The
nicotinic acetylcholine receptor (nAChR) subunit alpha-9 (CHRNA9) is a unique
cholinergic receptor, which is involved in
tumor proliferation, apoptosis,
metastasis and
chemotherapy resistance. However, the correlation between the expression level of CHRNA9 in
glioma and the clinical features and prognosis of
glioma patients has not been clarified. The aim of this study was to verify the expression level of CHRNA9 in
glioma and its effect on prognosis by bioinformatics methods. Methods: The
RNA-seq data of
glioma and normal samples were obtained from the TCGA and GTEx databases. Bioinformatics methods were utilized to analyze the differential expression of CHRNA9 between
tumor samples and normal samples. The potential association between CHRNA9 and the clinicopathological features of
glioma patients was also investigated. The Kaplan-Meier method and Cox regression were utilized to analyze the relationship between CHRNA9 expression level and survival time and prognostic value of
glioma patients. Enrichment analysis was applied to predict gene function and signaling pathways associated with CHRNA9. Experimental verification was performed using
tumor tissues and paracancerous tissues from
glioma patients. Results: The results of bioinformatics analysis showed that the expression of CHRNA9 was increased in
glioma tissues, correlating with poor prognosis and reduced patient survival time. Enrichment analysis suggested that CHRNA9 may interact with the JAK/STAT pathway. CHRNA9 was also found to be abnormally expressed in various other
tumors and associated with the expression levels of numerous immune checkpoints in
glioma. The findings from the analysis of clinical samples revealed that the expression levels of both
mRNA and
protein of CHRNA9 in
glioma tissues were higher than those in paracancerous tissues. Similarly, the
mRNA expression levels of STAT3,
IL-6, and TNF-α, which are crucial factors in the STAT3 pathway, were elevated in
glioma tissues compared to paracancerous tissues. Conclusion: CHRNA9 is a potential prognostic marker and
immunotherapy target for
glioma, with its mechanism of action potentially linked to the STAT3 pathway.