NO-sulindac, PC-3 prostate cancer cells and the Akt signalling pathway
Prostate Research Group, Edinburgh Cancer Research Centre, University of Edinburgh, reports in January 2009 Int J Cancer on their team’s efforts to “assess the effects and mechanism of action” of a non steroidal antiflammatory drug (NSAID) called NO-sulindac on the PC-3 prostate cancer cell line under hypoxic conditions.”
Hypoxia is the state in which body tissues, in this case cancer cells, are starved of sufficient oxygen. Prostate cancer tumor cells are found in a hypoxic environment, the authors explain, “which induces resistance to chemotherapy.”
NO-sulindac belongs to a class of NSAIDs, known as Nitric oxide-releasing NSAIDs, which for the past few years have been under investigation as promising anti-cancer and chemotherapy enhancing agents.
The Edinburgh group found that NO-sulindac, under both normal and oxygen starved conditions causes the type of advanced prostate cancer cells tested, PC-3, to self-destruct through apoptosis, and has some directly cell-killing, cytotox and anti-invasive effects on the cells. NO-sulindance interfered with normal signalling in the cancer cellwhich otherwise would make the cells able to tolerate oxygen-deprivation. “NO-sulindac directly inhibits the hypoxia response of PC-3 prostate cancer cells by inhibiting HIF-1alpha translation via the Akt signalling pathway. The ability of NO-sulindac to inhibit tumour adaption to hypoxia has considerable relevance to the future management of prostate cancer with the same cellular properties as PC-3.”
Sources
NO-sulindac inhibits the hypoxia response of PC-3 prostate cancer cells via the Akt signalling pathway. Stewart GD et al.
Int J Cancer. 2009 Jan 1;124(1):223-32.
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