TTDA inhibited apoptosis by regulating the p53-Bax/Bcl2 axis in glioma

The trichothiodystrophy group A protein (TTDA) functions in nucleotide excision repair and basal transcription. TTDA plays a role in cancers and serves as a prognostic and predictive factor in high-grade serous ovarian cancer; however, its role in human glioma remains unknown. Here, we found that TTDA was overexpressed in glioma tissues. In vitro experiments revealed that TTDA overexpression inhibited apoptosis of glioma cells and promoted cell growth, whereas knockdown of TTDA had the opposite effect. Increased TTDA expression significantly decreased the Bax/Bcl2 ratio and the level of cleaved-caspase3. TTDA interacted with the p53 gene at the -1959 bp and -1530 bp region and regulated its transcription, leading to inhibition of the p53-Bax/Bcl2 mitochondrial apoptosis pathway in glioma cells. These results indicate that TTDA is an upstream regulator of p53-mediated apoptosis and acts as an oncogene, suggesting its value as a potential molecular target for the diagnosis and treatment of glioma. •TTDA was up-regulated in glioma tissues and acted as an oncogene.•TTDA promoted cell proliferation and inhibited mitochondrial apoptosis in glioma cells.•TTDA inhibited glioma cell apoptosis through the p53-Bax/Bcl2 mitochondrial pathway.•TTDA was an upstream regulator of p53-mediated apoptosis and bound with the p53 gene to inhibit the transcription of p53.