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.
Furthermore, the anti-cancer effects of morphine could be reversed by naloxone. Morphine inhibits the expression of NF-κB, Bcl-2, cyclind1, and VEGF while enhancing the expression of Bax in the tumors. Our data showed that morphine effectively inhibited the tumor growth in the nude mice. The protein expression of NF-κB, Bcl-2/Bax, cyclind1, and VEGF was detected by immunochemistry staining and western blot. The mRNA expression levels of NF-κB, Bcl-2/Bax, cyclind1, and VEGF were assessed by semi-quantitative polymerase chain reaction (qPCR). The growth of the tumor was evaluated by its growth curves. 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). Previous studies have found that morphine could affect cancer development however, this effect is poorly understood. Morphine is commonly used to relieve severe pain that is often associated with cancer.
