FYN is overexpressed in human prostate cancer
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Edwin M Posadas1, Hikmat Al-Ahmadie, Victoria L Robinson
1Section of Hematology/Oncology, Department of Medicine, University of Chicago, IL, USA. eposadas@medicine.bsd.uchicago.edu
Objective:
To test the hypothesis that FYN, a member of the SRC family of kinases (SFKs), is up-regulated in prostate cancer, as FYN is functionally distinct from other SFKs, and interacts with FAK and paxillin (PXN), regulators of cell morphology and motility.
Materials And Methods:
Through data-mining in Oncomine (http://www.oncomine.org), cell-line profiling with immunoblotting, quantitative reverse transcription and polymerase chain reaction (RT-PCR) and immunohistochemical analysis, we described FYN expression in prostate cancer. The analysis included 32 cases of prostate cancer, nine of prostatic intraepithelial neoplasia (PIN) and 19 normal prostates. Samples were scored for the percentage of stained glands and intensity of staining (from 0 to 3). Each sample was assigned a composite score generated by multiplying percentage and intensity.
Results:
Data-mining showed an eight times greater FYN expression in prostate cancer than in normal tissue; this was specific to FYN and not present for other SFKs. Expression of FYN in prostate cancer cell lines (LNCaP, 22Rv1, PC3, DuPro) was detected using quantitative RT-PCR and immunoblotting. Expression of FYN and its signalling partners FAK and PXN was detected in human tissue. Comparing normal with cancer samples, there was a 2.1-fold increase in median composite score for FYN (P < 0.001) 1.7-fold increase in FAK (P < 0.001), and a doubling in PXN (P < 0.05). There was a 1.7-fold increase in FYN (P < 0.05) and a 1.6-fold increase in FAK (P < 0.01) in cancer compared with PIN.
Conclusions:
These studies support the hypothesis that FYN and its related signalling partners are up-regulated in prostate cancer, and support further investigation into the role of the FYN as a therapeutic target.
Insights
FYN, a kinase involved in cell movement, is significantly increased in prostate cancer tissues and cell lines. This finding suggests FYN could be a potential therapeutic target for prostate cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- SRC family kinases (SFKs) play roles in cell signaling.
- FYN is a distinct SFK interacting with cell morphology regulators FAK and paxillin (PXN).
Purpose of the Study:
- To investigate the hypothesis that FYN is upregulated in prostate cancer.
- To examine the expression of FYN and its signaling partners FAK and PXN in prostate cancer.
Main Methods:
- Data-mining using Oncomine.
- Cell-line profiling via immunoblotting and quantitative RT-PCR.
- Immunohistochemical analysis of prostate cancer tissues (32 cases), PIN (9 cases), and normal prostates (19 cases).
Main Results:
- FYN expression was eight times higher in prostate cancer than normal tissue, specific to FYN.
- Increased expression of FYN, FAK, and PXN was observed in prostate cancer compared to normal tissue.
- FYN and FAK showed increased expression in cancer compared to PIN samples.
Conclusions:
- FYN and its signaling partners are upregulated in prostate cancer.
- Further research into FYN as a potential therapeutic target for prostate cancer is warranted.
