Exogenous Morphine Inhibits Human Gastric Cancer MGC-803 Cell Growth by Cell Cycle Arrest and Apoptosis Induction

• DOI: 10.7314/apjcp.2012.13.4.1377
• Publication Date: 2012-09-06T20:33:01Z
• Authors: Yi Qin; Jing Chen; Li Li; Chun-Jie Liao; Yu-Bing Liang; En-Jian Guan; Yu-Bo Xie
• Keywords: 0301 basic medicine; Analysis of Variance; Morphine; Caspase 3; Cell Survival; Survivin; Carcinoma; NF-kappa B; Gene Expression; Apoptosis; Caspase 9; Inhibitor of Apoptosis Proteins; 3. Good health; Analgesics, Opioid; G2 Phase Cell Cycle Checkpoints; 03 medical and health sciences; Stomach Neoplasms; Cell Line, Tumor; Microscopy, Electron, Scanning; Humans; RNA, Messenger; Cell Proliferation

Morphine is not only an analgesic treating pain for patients with cancer but also a potential anticancer drug inhibiting tumor growth and proliferation. To gain better insight into the involvement of morphine in the biological characteristics of gastric cancer, we investigated effects on progression of gastric carcinoma cells and the expression of some apoptosis-related genes including caspase-9, caspase-3, survivin and NF-κB using the MGC-803 human gastric cancer cell line. The viability of cells was assessed by MTT assay, proliferation by colony formation assay, cell cycle progression and apoptosis by flow cytometry and ultrastructural alteration by transmission electron microscopy. The influences of morphine on caspase-9, caspase-3, survivin and NF-κB were evaluated by semi-quantitative RT-PCR and Western blot. Our data showed that morphine could significantly inhibit cell growth and proliferation and cause cell cycle arrest in the G2/M phase. MGC-803 cells which were incubated with morphine also had a higher apoptotic rate than control cells. Morphine also led to morphological changes of gastric cancer cells. The mechanism of morphine inhibiting gastric cancer progression in vitro might be associated with activation of caspase-9 and caspase-3 and inhibition of survivin and NF-κB.