The Role of Celecoxib as a Cox-2 Inhibitor Increasing the Radiosensitivity of Tumor Tissue

Abstract

One of the major causes of death in the world is cancer. Due to significant advances in molecular and cellular biology, previous approaches in cancer treatment have progressed, applying new strategies. Identification and use of chemotherapy and radiation sensitizers and their effect on the further destruction of the cancer cells have received a lot of attention in medical studies. The main objectives of this Review Article are to identify the inhibitors of the enzyme COX -2 and mechanisms that are known to inhibit the enzyme in order to increase the sensitivity of tumour cells to radiation. COX-2 enzyme inhibition with Celecoxib and the prevention of the restoration of this tumour have been a major challenge for researchers. Evidence Acquisition: The mechanism by which the cells are radio sensitized can increase the initial damage, inhibiting the restoration and redistribution of the cell cycle as well as blocking in the more radio sensitized zone. Enhanced response to treatment would be initiated by identifying enzymes that are involved in increasing tumour growth and followed by inhibiting tumour growth and restoration. COX-2 is one of the enzymes expressed highly in tumour growth. Inhibiting this enzyme will enhance the response rate of treatment followed by the death of tumour cells. High expression of COX-2 gene in tumours is more related to tumour aggressive behaviour and a worse prognosis. Results: There are five mechanisms that the COX-2 enzyme applies to develop tumours and increase the malignant phenotype of tumour cells: 1- Apoptosis inhibition 2- Angiogenesis increase 3- Invasion rise 4- Inflammation modulation/weakened immunity, suppression 5- Procarcinogen conversion to carcinogens. Known mechanisms in increased sensitivity to radiation by Celecoxib: 1-COX-2 inhibition and subsequent reduction in PGE2 production result in increasing apoptosis and decreasing angiogenesis proliferation.2. The mechanism of COX-2 inhibition by Celecoxib has not been fully recognized. The drug inhibits the COX-2 enzyme through TNF-α signalling by nuclear transfer inhibition of growth factor. It also inhibits NF-KB transcription factor activation. Apoptosis inhibition is one of the mechanisms implemented by COX-2 that increases tumourigenesis. Cell cycle arrest at G1-S is one of the most sensitized areas to radiation. Studies in the field of pancreatic and ovarian carcinoma cells show cell cycle arrest at G1-S; the mechanism by which this arrest happens is not fully understood. Conclusions: Celecoxib, as a COX-2 inhibitor that affects and inhibits some enzymes and creates changes in the cell cycle process, has the role of a radiosensitizer. Celecoxib prevents cancer. Celecoxib inhibits tumour growth delay and the amount is insignificant. Simultaneous application of radio sensitzers such as celecoxib and chemo radiotherapy procedures will have a more damaging effect on the tumour cells.