Abstract
Morphine is commonly used to relieve severe pain that is often associated with cancer. Previous studies have found that morphine could affect cancer development; however, this effect is poorly understood. To further clarify the anti-cancer potential of morphine for the development of cancer in vivo, we observed how morphine affects the growth of human gastric tumor in a murine xenografting model and the expression of NF-κB and its downstream target genes (Bcl-2/Bax, cyclind1, and VEGF). The growth of the tumor was evaluated by its growth curves. The mRNA expression levels of NF-κB, Bcl-2/Bax, cyclind1, and VEGF were assessed by semi-quantitative polymerase chain reaction (qPCR). The protein expression of NF-κB, Bcl-2/Bax, cyclind1, and VEGF was detected by immunochemistry staining and western blot. Our data showed that morphine effectively inhibited the tumor growth in the nude mice. Morphine inhibits the expression of NF-κB, Bcl-2, cyclind1, and VEGF while enhancing the expression of Bax in the tumors. Furthermore, the anti-cancer effects of morphine could be reversed by naloxone. The mechanism might be associated with the action of opioid receptors that downregulate the expression of NF-κB leading to the regulation of the downstream target genes (Bcl-2/Bax, cylind1, and VEGF) in the tumors.