Expression of scatter factor and c‐ met receptor in benign and malignant breast tissue

Abstract

SF and c-met are overexpressed in breast carcinoma as compared with benign breast tissue, and they tend to be coexpressed in cancerous tissue. These findings are consistent with the idea that the SF:c-met ligand:receptor pair may have a role in breast carcinoma progression.

Co‐expression of hepatocyte growth factor and c‐Met predicts peritoneal dissemination established by autocrine hepatocyte growth factor/c‐Met signaling in gastric cancer

“…Indeed, co-expression of HGF and c-Met has been detected in a variety of human tumors. 35,36 Park et al 37 have screened 43 primary gastric carcinomas immunohistochemically and found that 13 showed both HGF and c-Met signals in tumor cells, which suggests the presence of HGF/c-Met autocrine signaling in gastric cancer. However, the possibility cannot be ruled out that the HGF protein detected in tumor cells originates from neighboring fibroblasts.…”

Ras effector pathways modulate scatter factor-stimulated NF-κB signaling and protection against DNA damage

“…SF was found to protect epithelial, carcinoma and glioma cells against DNA damaging agents, including adriamycin (ADR, a DNA topoisomerase IIa inhibitor), ionizing radiation, cisplatinum (a DNA cross-linking agent), and other agents (Fan et al, 1998(Fan et al, , 2001Bowers et al, 2000). These findings may be significant because expression of SF and c-Met are upregulated in various tumor types (e.g., breast cancers, gliomas and bladder cancers) (Jin et al, 1997;Rosen et al, 1997). Thus, the accumulation of SF and c-Met might contribute to chemoresistance and radioresistance of the tumors.…”

Scatter factor protects epithelial and carcinoma cells against apoptosis induced by DNA-damaging agents

“…Overexpression of SF induces in various experimental tumor models, including a human breast cancer model, causes enhanced in vivo tumorigenicity, tumor growth, and angiogenesis (Rong et al, 1992;Lamszus et al, 1997;Laterra et al, 1997). In addition, studies of clinical human breast cancer specimens indicate that SF and cMet receptor are over-expressed during the progression from benign proliferative lesions or non-invasive tumors to invasive carcinomas (Yao et al, 1996;Jin et al, 1997). Within the invasive cancer group, the SF content was strongly correlated with the content of von Willebrand's factor, an endothelial cell marker, suggesting a relationship between SF and tumor vascularity (Yao et al, 1996).…”