Abstract
Radiation is omnipresent in our surrounding and continuously interacts with us. However, overexposure of ionizing radiation during medical procedures and nuclear accidents has serious concern all over the world. Radiation interacts with biological tissues and deposit its energy resulting in massive oxidative stress leading to cell death. As a result of radiation induced oxidative stress, several pro-survival cell signaling pathways gets activated that provide survival advantages to cancer cells. The predominant signaling pathways that activated upon irradiation include inflammation, cell cycle checkpoints arrest, DNA repair, and apoptosis inhibition. These major signaling pathways are induced through other connected pathways such as PI3K, AKT, ERK Kinase/ERK, Ras, RAF, MEK, phospholipase C/protein kinase C, NfKB, HIF1α, and Jak/STAT pathways and thus decide the fate of the cells. Comparatively, normal cells did not show radioresistance probably due to their controlled proliferation, regulated transcription, and normal metabolism. Hyper activation of cancer cells makes them prone to induce pro-survival signaling resulted radioresistance. Therefore, by identification and validation and evaluation of pro-survival pathways inhibiting drugs in appropriate experimental model may provide a logical solution for more efficient radiotherapy outcome. Whereas, development of pro-survival pathway activators may provide radioprotection to the surrounding normal cells and tissues.
Keywords
Apoptosis, Cell signaling, Oxidative stress, DNA damage, Inflammation