Green tea consumption is associated with protective and preventive effects against various types of cancer. These effects are attributed to polyphenols, particularly epigallocatechin-3-gallate (EGCG). EGCG acts by directly inhibiting tumor suppressor protein p53. The binding mechanism by which EGCG inhibits p53 activity is associated with residues Trp23-Lys24 and Pro47-Thr55 within the p53 N-terminal domain (NTD). However, the structural and thermodynamic aspects of the interaction between EGCG and p53 are poorly understood. Therefore, based on crystallographic data, we combine docking, molecular dynamics (MD) simulations, and molecular mechanics generalized Born surface area approaches to explore the intricacies of the EGCG-p53 binding mechanism. A triplicate microsecond MD simulation for each system is initially performed to capture diverse p53 NTD conformations. From the start, the most populated cluster of the second run (R2-1) stands out due to a unique opening between Trp23 and Trp53. During MD simulations, this conformation allows EGCG to sustain a high level of stability and affinity while interacting with both regions of interest and deepening the binding pocket. Structural analysis emphasizes the significance of pyrogallol motifs in EGCG binding. Therefore, the conformational shift in this gap is pivotal, enabling EGCG to impede p53 interactions and manifest its anticancer properties. These findings enhance the present comprehension of the anticancer properties of green tea polyphenols and pave the way for future therapeutic developments.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11080030 | PMC |
http://dx.doi.org/10.1021/acsomega.3c10523 | DOI Listing |
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