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Opioids, acting via G-protein coupled membrane receptors, induce analgesia. However their role is not limited to their anti-nociceptive action. They are found in several peripheral tissues acting as negative regulators of cellular processes. Even though that is not fully elucidated, it becomes obvious that opioids exert their effects in close relation to other neuropeptides such as somatostatin. Hepatocellular carcinoma is one tumor, among others, which secrete bioactive peptides while somatostatin analogs exert an inhibitory effect. We have used the human hepatocyte-derived cancer cell line HepG2, in order to examine the effect of opioids on cell growth and their possible mode of action. Our results show that the opioid ethylketocyclazocine (EKC) inhibits cell proliferation and induces apoptosis. This inhibitory effect is not exerted via opioids receptors since it was not reversed by the opioid antagonist diprenorphine and functional opioid receptors were not found on HepG2 cells. On the contrary, we show that EKC binds to somatostatin receptors, and activates a PTP signalling cascade. In this respect, the interaction of opioids with somatostatin receptors on hepatocellular carcinoma cells, and the fact that they are widely used for pain control, may provide some additional clues for the discrepancies during treatment with somatostatin analogues.
Pubmed ID: 17113072
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The goal is to understand as completely as possible the relationships between sets of inputs and outputs in signaling cells that vary both temporally and spatially. The same goal, stated from a slightly different perspective, is to understand fully how cells interpret signals in a context-dependent manner. This will involve identification of all the proteins that comprise the various signaling systems, the assessment of time-dependent information flow through the systems in both normal and pathological states, and finally the reduction of the mass of detailed data into a set of interacting theoretical models that describe cellular signaling. Sponsors: The AfCS Project was conceived under the Glue Grant Initiative of the National Institute of General Medical Sciences. Support is received from the National Institute of General Medical Sciences and the National Institute of Allergy and Infectious Diseases. Keywords: Alliance, Cellular, Signaling, Temporally, Spatially, Cell, Model,
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