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BookmarkScienceDaily (July 2, 2008) — For men, one of the leading causes of death from cancer is prostate cancer that has spread to a second site (something known as metastatic prostate cancer).
Defining the molecular mechanisms by which the initial tumor becomes able to spread to a new site (a process known as metastasis) is likely to help clinicians predict an individual's chance of survival and help researchers develop new therapies.
New data, generated by John Martignetti and colleagues, at Mount Sinai School of Medicine, New York, has identified a specific form of the protein KLF6 (KLF6-SV1) as indicative of poor survival in men with prostate cancer.
The information in genes is converted into a protein via an intermediate known as mRNA. In the study, analysis of tumors from men with localized prostate cancer who had undergone a prostatectomy revealed that increased levels of an mRNA intermediate involved in the generation of KLF6-SV1 correlated with more rapid disease recurrence and decreased survival.
Consistent with this having an important role in metastasis, prostate cancer cells expressing increased levels of KLF6-SV1 metastasized more rapidly and more often than normal prostate cancer cells in two mouse models of metastatic prostate cancer.
Conversely, decreasing KLF6-SV1 expression in prostate cancer cells decreased tumor growth in mice. The authors therefore suggest that measuring KLF6-SV1 expression levels in prostate cancer tumors at the time of diagnosis might help clinicians predict whether or not the tumor will metastasize and that targeting KLF-SV1 might provide a new avenue for the development of therapeutics to treat individuals with prostate cancer.
Story Source:
Adapted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
Journal Reference:
- Goutham Narla et al. KLF6-SV1 overexpression accelerates human and mouse prostate cancer progression and metastasis. Journal of Clinical Investigation, July 1, 2008
Note: If no author is given, the source is cited instead.
