Exogenous morphine inhibits the growth of human gastric tumor in vivo

被引：9

作者：

Li, Chunlai ^{[1
]}

Li, Li ^{[1
]}

Qin, Yinying ^{[1
]}

Jiang, Yage ^{[1
]}

Wei, Yi ^{[1
]}

Chen, Jing ^{[1
]}

Xie, Yubo ^{[1
]}

机构：

[1] Guangxi Med Univ, Affiliated Hosp 1, Dept Anesthesiol, 6 Shuangyong Rd, Nanning 530021, Peoples R China

来源：

ANNALS OF TRANSLATIONAL MEDICINE | 2020年 / 8卷 / 06期

关键词：

Morphine; gastric cancer; nude mice; tumor growth; NF-kappa B; CANCER PROGRESSION; OPIOID RECEPTOR; ANGIOGENESIS; APOPTOSIS; CELLS; METASTASIS; RECURRENCE; PROMOTES;

D O I：

10.21037/atm.2020.03.116

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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-kappa B 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-kappa B, Bcl-2/Bax, cyclind1, and VEGF were assessed by semi-quantitative polymerase chain reaction (qPCR). The protein expression of NF-kappa B, 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-kappa B, 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-kappa B leading to the regulation of the downstream target genes (Bcl-2/Bax, cylind1, and VEGF) in the tumors.

引用

页数：7

共 27 条

[1] Morphine sulfate inhibits hypoxiainduced vascular endothelial growth factor expression in endothelial cells and cardiac myocytes [J].