Spread of prostate cancer can be halted by disrupting communication between cancer cells and the cells that promote inflammatory response, researchers at Northwestern University Feinberg School of Medicine have found.
The finding not only suggests new ways to control cancer spread and metastasis but also provide an impetus to look more closely at existing inflammation-controlling drugs including non-steroidal anti-inflammatory drugs, cyclooxygenase inhibitors, antioxidants and statins.
AdvertisementDr. Paul Lindholm said it is possible that these widely available drugs could be used to control aggressive cancer cell growth and spread for these and other inflammation-associated cancers.
In previous studies, Dr. Lindholm and his colleagues at Northwestern found that when compared to benign prostate tissues, prostate cancer tissue has a higher density of macrophages and the monocytes from which these immune system cells derive.
These scavenger cells are vital to the regulation of immune responses and the development of inflammation.
High grade and high stage prostate cancer tissues showed significantly increased numbers of macrophages compared to low grade and low stage tumours.
When the researchers added monocyte-like cell lines or monocytes obtained from the blood of normal people to less aggressive prostate cancer cell lines, these cancer cells became more invasive, indicating that the cancer cells and the monocytes were indeed communicating with each other.
In the new study, the researchers showed that the monocyte-like cells stimulate the cancer cells' Nuclear Factor-kappaB, a gene regulating transcription factor able to stimulate gene activity.
To check whether NF-kappaB activity was boosting the cancer cells' movement and invasive activity, the researchers introduced into the cancer cells biological inhibitors that blocks NF-kappaB activity.
The treatments that block NF-kappaB activity reduced the cancer cell movement and invasion through the basement membrane (a thin, delicate layer of connective tissue underlying the epithelium of many organs).
The study was presented on April 8 at the Experimental Biology 2008 meeting in San Diego.
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