AGCF2 exhibits cell type-dependent differential functions, contributing to glia-dependent angiotensinogen promoter activity.
Cell-type specific AGCF2 effects on angiotensinogen promoter warrant caution in clinical translation; leaves open glia-dependent mechanisms for further validation.
To investigate the regulatory mechanisms of human angiotensinogen (ANG) gene expression in the brain, we analyzed the 1.3-kb promoter by transfection studies and gel shift assays. The region from -106 to +44 was sufficient for promoter activity in glioblastoma cells, and multiple nuclear factors including AGCF2 (human ANG core promoter binding factor 2) bound within this 150-bp region. The mutations within AGCF2-binding elements decreased the transcriptional activity in glioblastoma cells but rather increased it in hepatoma cells. These results indicate that AGCF2 has a differential function between these cells and contributes to the glia-dependent angiotensinogen promoter activity.
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Yanai et al. (1997) studied this question.
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