Screening method for inhibiting angiogenesis targets through celecoxib

Abstract

The invention belongs to the field of treating tumor diseases, and particularly relates to a screening method for inhibiting angiogenesis targets through celecoxib. According to the method, by selecting protein expressed by 84 genes on a blood vessel formation polymerase chain reaction chip as a potential receptor protein database (PDB), the PDB and a UniProt database are used for screening 54 receptor protein structures, MGLTools is used for processing the receptor protein structures, after a molecular docking box is constructed, Autodock_vina is used as a molecular docking tool to calculatethe free energy of the binding site of the celecoxib and each protein receptor, and the protein receptors with the binding site free energy smaller than 9.0 kcal / mol are selected as potential targets.

Description

technical field [0001] The invention belongs to the field of treating tumor diseases, and in particular relates to a screening method for celecoxib to inhibit angiogenesis targets. Background technique [0002] Celecoxib has been reported to promote cell apoptosis and inhibit angiogenesis, thereby inhibiting tumor growth. Its anti-angiogenic effect is generally considered to be related to the inhibition of cyclooxygenase-2 (COX-2) activity. However, our previous studies found that different concentrations of celecoxib could not block the increase of COX-2 activity after radiotherapy. Therefore, celecoxib may inhibit angiogenesis through a COX-2-independent pathway, that is, an off-target effect (Off- target) to achieve. Recent studies support our finding that there is a COX-2-independent pathway for the antitumor effect of celecoxib. It is generally believed that celecoxib inhibits the synthesis of prostaglandin PGE2 by inhibiting the activity of COX-2, thereby blocking t...

AI Technical Summary

Problems solved by technology

It is generally believed that celecoxib inhibits the synthesis of prostaglandin PGE2 by inhibiting the activity of COX-2, thereby blocking tumor growth; Rofecoxib, more potent at inhibiting COX-2 but less potent at suppressing tumors

At the same time, adding a methyl group to celecoxib, 2,5-dimethyl-celecoxib (DMC), lost the ability to inhibit COX-2, but it can almost completely mimic the tumor suppressor function of celecoxib

In addition, the randomized controlled study of Celecoxib concurrent radiotherapy for lung cancer resulted in negative results due to failure to complete the expected enrollment. The important reason is the lack of COX-2-independent biomarkers and selective inclusion of subjects

Images