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- W2957444282 abstract "466 Hepsin is a type II transmembrane serine protease documented to be up regulated in prostate cancer (1), and implicated in other cancers such as renal cell carcinoma and ovarian cancer. Hepsin expression has additionally been correlated with progression of prostate cancer and poor prognosis (2). An in vivo model has demonstrated a role for hepsin in basement membrane degradation and prostate cancer metastasis (3) but exactly how hepsin promotes metastasis is not clear. One known substrate for hepsin is Hepatocyte Growth Factor (HGF) (4). Expression of HGF and its receptor c-Met, are associated with tumor progression in prostate cancer, as well as other cancer types. HGF and c-Met have also been associated with the progression of prostate tumors to an androgen-independent state (5). In order to better understand how hepsin contributes to prostate tumor development and the metastatic process, we have investigated the phenotypic effects of stably over-expressing human Hepsin in PNT2 cells, a human prostate epithelial cell line. Hepsin expressed by the stable cell line was demonstrated to be active in a protease assay. Using colony formation assays to assess cell survival and proliferation, we have demonstrated that over expression of hepsin does not affect cell survival but instead leads to a decrease in the rate of cell proliferation as determined by colony area (p To more accurately mimic an in vivo setting, we have cultured control or hepsin expressing PNT2 cells as 3D spheroids. These were co-cultured with osteoblast cells, since osteoblasts are reported to produce pro-HGF and prostate cancer commonly metastasizes to the bone. Hepsin expression altered the morphology and growth of the spheroids, with Hepsin expression leading to increased proliferation and invasive properties of the cells. In conclusion, expression of Hepsin in prostate epithelial cells leads to increased cell motility and migration, altered cell morphology and promotes growth in the presence of essential factors provided by osteoblasts. We believe that in prostate cancer, these changes contribute to the metastatic process and aid tumor growth at metastatic sites. We are currently using a number of in vivo models in order to confirm these observations. (1) Magee et al (2001) Cancer Res. 61: 5692-5696 (2) Xuan et al (2006) Cancer Res. 66: 3611-3619 (3) Klezovitch et al (2004) Cancer Cell 6: 185-195 (4) Herter et al (2005) Biochem J. 390: 125-136 (5) Maeda et al (2006) BBRC. 347: 1158-1165" @default.
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- W2957444282 date "2007-05-01" @default.
- W2957444282 modified "2023-09-26" @default.
- W2957444282 title "In vitro evidence for the role of hepsin in metastatic prostate cancer" @default.
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