Celecoxib Induces Apoptosis And Impotives The Expression Of VEGF Though ER Stress In Human Colorectal Cells

In the present study, we take the human colorectal cells HCT116and HT-29as ourobject of the research. The non-steroidal anti-inflammatory drug， celecoxib is used to treatcells, disclosing the mechanism of celecoxib upregulating the expression of VEGF inHCT116and HT-29. We would provide experimental basis for the using of celecoxib infield of anti-tumor therapy applications.Object: By studying the non-steroidal anti-inflammatory drug， celecoxib is used totreat cells, disclosing the mechanism of celecoxib upregulating the expression of VEGF andanti-tumor, providing experimental basis for the using of celecoxib in field of anti-tumortherapy applications.Methords: Utilizing Western Bloting to detect the expression of VEGF andGRP78/BIP, the marker protein of ERS, and CHOP, the the marker protein of apoptosis byERS. Making use of Flow Cytometry to measure the rate of cell apoptosis.Results: When using high-dose celecoxib to treat HCT116and HT-29, theexpression of VEGF，GRP78and CHOP increase. In addition, the rate of cell apoptosis ofHCT116and HT-29also adding by dose-response by Flow Cytometry Alpha.But whenadding PBA (the depressor of ERS),the expression of VEGF， GRP78and CHOPincreassion by celecoxib is disappearing.Conclusions：Celecoxib induces the ERS and promotes cell apoptosis. Both apoptosisand up-regulation of VEGF via activation of the ERS response. The increase of expressionof VEGF may result the resistance of drug. Further studies are necessary to evaluate whether the combi-nation of celecoxib with anti-VEGF agents is a promisingtherapeutic modality for cancer.