Effect of Active Compound of Pasak Bumi Root (Euricoma longifolia, Jack) as an inhibitor of CDK2 methylation: In Silico Study

Abstract

Active compound of Pasak Bumi’s root, a native plant of Indonesia, is used as antitumor by triggering cell apoptosis and reactivating the silence tumor suppressor gene caused by hypermethylation, inhibiting cancer cell proliferation. The aim of this study is to know the role of quassinoid from Pasak Bumi’s root (Eurycoma longifolia Jack) as an inhibitor of CDK2 methylation in silico. This is a descriptive study. CDK2 samples are obtained from Protein Data Bank (RSCB.org) with ID3SWR, samples of natural quassinoid are obtained from PUBCHEM NCBI and controlled by Sunitinib (®Sutent). Autodock Vina program PyRx 0.8 is used to analyze Molecular Docking. The process of analyzing molecular interactions is carried out using the LigandScout V.2.0 program. Visualization process are carried out using LigandScout V.2.0 program. The affinity of quassinoid and sutinab to CDK are -6.1 and -9.4, respectively. The more negative the binding affinity value, the better the ability of the compound (ligand) to bind to the receptor (macromolecules). From this case, Sutinab has better value compared to quassinoid. Target protein analysis using HITPICK shows quassinoid’s target predictor is JUN protein. Protein interaction analysis are obtained, and the compound is using stitch. JUN protein and Sunitib could bind with CDK2. The conclusion of this study is Sutinib has greater affinity compared to quassinoid.

Apoptosis Potency Prediction of Steroid Saponin from Gembili (Dioscorea esculenta) as Bcl-2 and Bcl-xL Inhibitors in Colon Cancer

“…The results were docking indicated by the lowest binding affinity of the interaction between the ligands and the receptor protein. The smaller or negative the binding affinity, the greater the ability of the ligands to bind to the receptors [26].…”