Non-small-cell lung cancer (NSCLC), occupying a great proportion of lung cancer, threatens the health of patients, and the cyclooxygenase-2 (COX-2) expression is found to be upregulated in lung cancer. Pterostilbene (PTE) is perceived as a novel method for clinical therapy due to its high performance. However, the mechanism underlying and the interaction between PTE and COX-2 remain vague. We simulated radiation circumstances and transfected cells with the interference of PTE and COX-2. Our results showed that radiation or PTE treatment alone restrained cell proliferation and viability while stimulating cell apoptosis, and the above properties were strengthened when the two were in combination. The COX-2 expression was promoted by radiation but was reduced by PTE. PTE reversed the effects of radiation on the COX-2 expression. COX-2 knockdown suppressed COX-2 expression and proliferation and enhanced apoptosis of cells suffering radiation, while COX-2 overexpression reversed the inhibition of PTE. Our study suggested PTE regulated NSCLC cell proliferation and apoptosis via targeting COX-2, which might shed a light on cancer therapy.
Keywords: COX-2; apoptosis; non-small-cell lung cancer; proliferation; pterostilbene; radiotherapy.
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