A Molecular Analysis of Homo Sapiens’ Tumor-causing TP53 gene and associated P53 protein via Bioinformatics pipeline

Objective: The current study investigates characteristics and post-translational modification (PTM) sites of TP53  and its encoding protein (P53) through a bioinformatics pipeline. The findings of this study will provide a gateway to novel therapeutics strategies against numerous cancers followed by TP53 in humans. Methods: In this study, we utilized in-silico strategies to evaluate the PTM site response in P53 protein leading to cancer treatment. PSIPRED online tool predicted the secondary structure of P53 and interpret its robustness to mutation. ProtParam determined the characterized physiology and NetPhos v3.1 combined with Phos3D provided possible phosphorylation sites of P53. N- and O-glycosylation site identification evaluated by NetNGlyc 1.0 and NetOGlyc 4.0 servers, which is an important factor in determining cancerous activity level. YinOYang v1.2 predicted possible Yin-Yang sites involved in the carcinogenic activity of P53. Results: Human P53 protein has 42 phosphorylation sites (30 Ser + 11 Thr + 1 Tyr) followed by several kinases involved in its transcriptional activity. A total of 16 O-glycans and 2 N-glycans are determined in P53 protein. However, 8 possible YinYang sites are also predicted, which are involved in the oncogenic nature of P53 protein. Conclusions: TP53 genes are responsible for several cancers in humans, especially like i-Fraumeni (LFL) syndrome. Its encoding protein P53 shows carcinogenic activity in the human body. Several predicted YinYang sites as well as N- and O-glycans are involved in P53 protein’s carcinogenic behavior. These findings will be helpful in the treatment of cancer patients by targeting these identified sites.