| dc.description.abstract | Background: Retinoblastoma occurs due to gene mutations that have the potential to cause death. Retinoblastoma occurs due to mutations in the allele of the Retinoblastoma gene (RB1) which acts as a tumor suppressor gene, causing retinal cells to undergo uncontrolled proliferation. Mutations in the RB1 gene due to changes in the coding of this gene indirectly cause overexpression of the CDK4 and CDK6 proteins. curcumin can inhibit the proliferation of cancer cells, inhibit angiogenesis, inhibit metastasis, trigger apoptosis and increase the sensitivity of chemotherapy and radiotherapy. Curcumin induces Y79 cell apoptosis through activation of the JNK and p38 MAPK pathways. Purpose: analyzed the potential of curcumin in the treatment of retinoblastoma by examining its binding to CDK4, CDK6 and pRB proteins in In Silico with molecular docking techniques. Methods: The structure of the CDK4, CDK6, pRb receptors in the form of *.pdb was converted into *.pdbqt format through the AutoDock Tools 1.5.6 program. The docking method is done by tethering the ligand to the CDK4, CDK6, pRb receptors. The mooring coordinates are CDK4 (Grid Center) x = 13.0, y = 8.836, z = 43.2 and Grid Box size x= 70, y= 64, z= 62 . The mooring coordinates are CDK6 (Grid Center) x = 11,533, y = 25,223, z = 0.104 and Grid Box size x= 72, y= 66, z= 68 . The mooring coordinates are pRb (Grid Center) x = 33,576, y = 13.979, z = 21,171 and Grid Box size x= 84, y= 58, z= 64. Result: Curcumin has a binding affinity value for CDK4, CDK6, pRb proteins of -7.7, -7.8, -7.1. Conclusion: Curcumin has potential as a drug candidate for retinoblastoma. | en_US |
