Description
Radiation therapy is widely used in cancer treatment; however, many cancer cells develop resistance by activating adaptive stress and survival pathways. Understanding the early cellular responses to radiation stress remains an important question in cancer biology. In this study, we asked: what metabolic adaptations do cancer cells maintain during the early stages of radiation-induced stress? To address this question, we used PANC-1 pancreatic cancer cells as a model system and examined the effects of ultraviolet radiation (UVR) on cellular signaling and mitochondrial protein expression. Cells were exposed to UVR at 20, 40, and 80 minutes to evaluate time-dependent cellular responses. Based on preliminary observations, a 40-minute exposure was selected for protein analysis because it produced measurable cellular stress while maintaining viable cells. By immunoblotting analysis, we observed a decrease in phosphorylation of mechanistic target of rapamycin (mTOR) and an increase in phosphorylation of c-Jun N-terminal kinase (JNK), indicating suppression of growth signaling and activation of cellular stress pathways. We then examined mitochondrial respiratory proteins ATP synthase subunit alpha (ATP5A) and succinate dehydrogenase subunit A (SDHA) and observed no detectable changes in their expression. This preliminary study suggests that cancer cells maintain mitochondrial respiratory function during early radiation-induced stress, which may represent an adaptive survival response.