Study On Follistatin - Like Protein 1 Through EMT Pathway In Bone Metastasis Of Prostate Cancer

Prostate cancer remains the most prevalent type of malignancies and frequent cause of cancer-related mortality in male population in Western counties. Although the incidence of prostate cancer in China is relatively low compared to Western countries, the rate of incidence has rapidly increased recently. The three following factors may be related to this rising trend:(1) more and more patients with PCa were identified as population aging intensified.(2) in consequence of the westernization of life habits and diet, the incidence of PCa was increasing.(3) wide application of prostate specific antigen screening,more PCa patients who could not be detected before could be identified in early stage now. Bone is the most common site of PCa metastasis. It is reported 80%-90% patients with advanced prostate cancer would develop bone metastasis. The related mechanism of bone metastasis is still unclear. Many literatures reported prostate cancer cells can produce numerous cytokines, such as TGF-β 、 FGF 、 EGF and so on, which can stimulate the proliferation and differentiation of bone cell. Follistatin-like 1 protein(FSTL1) is one of extracellular matrix proteins. It is involved in cell proliferation, differentiation and metabolism. In recent years, the role of FSTL1 in inflammation, autoimmune disease and tumor had been preliminary studied, but its function in bone metastasis remains unclear. In our study, the expression level of prostate cancer cell lines from different sources was detected. PC-3 which originates from bone metastasis lesions showed an extremely higher FSTL1 expression than other cell lines. Therefore we concluded that FSTL1 may play an important role in bone metastasis. Then after transfected with small interfering RNA(SiRNA) targeting FSTL1, the migration of PC-3 cells was significantly depressed. Consulting pertinent literatures, it is indicated epithelial-mesenchymal transition(EMT) signal pathway was involved in bone metastasis induced by FSTL1, which was confirmed by our following experiment.Taking together, a relative high expression of FSTL1 was detected in PC-3 cell lines which originated from bone metastasis lesions. Targeting FSTL1 would prevent cell migration in a EMT pathway.FSTL1 may play an crucial part in bone metastasis which prompts FSTL1 targeted therapy would provide a new optional clinical treatment for prostate cancer bone metastasis.