Aquaporin 1 overexpression may enhance glioma tumorigenesis by interacting with the transcriptional regulation networks of Foxo4, Maz, and E2F families

The glioblastoma has served as a valuable experimental model system for investigating the growth and invasive properties of glioblastoma. Aquaporin-1 (AQP1) in facilitating cell migration and potentially contributing to tumor progression. In this study, we analyzed the role of AQP1 overexpression in glioblastoma and elucidated the main mechanisms involved.

AQP1 may be implicated in glioma formation by interacting with the transcriptional regulation networks involving the FOXO4, MAZ, and E2F1/2. These findings shed light on the potential significance of AQP1 in glioma pathogenesis and warrant further investigations to unravel the underlying molecular mechanisms.

AQP1 overexpression recombinant vector was introduced into C6 rat glioma cells to construct an AQP1 overexpression C6 cell line, and its effect on cell viability and migration ability was detected by MTT and Transwell. RNA was extracted by Trizol method for gene sequencing and transcriptomics analysis, and the differentially expressed genes (DEGs) were enriched for up- and downregulated genes by Principal component analysis (PCA), and the molecular mechanism of AQP1 overexpression was analyzed in comparison with the control group using the NCBI GEO database. Statistical analysis was performed using Mann-Whitney paired two tailed t test.

The cell viability of AQP1-transfected cell lines increased by 23% and the mean distance traveled increased by 67% compared with the control group. Quantitative analysis of gene expression showed that there were 12,121 genes with an average transcripts per million (TPM) value greater than 1. DEGs accounted for 13% of the genes expressed, with the highest correlation with upregulated genes being FOXO4 and MAZ, and the highest with downregulated genes being E2F TFs. Conclusions: AQP1 may be implicated in glioma formation by interacting with the transcriptional regulation networks involving the FOXO4, MAZ, and E2F1/2. These findings shed light on the potential significance of AQP1 in glioma pathogenesis and warrant further investigations to unravel the underlying molecular mechanisms.