expression correlates with decreased metastasis and increased survival in a high-grade serous ovarian cancer xenograft murine model.

The cause of death among high-grade serous ovarian cancer (HGSOC) patients involves passive dissemination of cancer cells within the peritoneal cavity and subsequent implantation of cancer spheroids into adjacent organs. () encodes a type I transmembrane protein containing several functional domains inherent to adhesion molecules. Previous studies using methods have indicated that functions as a tumor suppressor in several cancers, including HGSOC. In this study, we generated a HGSOC xenograft mouse model to investigate expression in the context of HGSOC late-stage metastasis and overall survival. OVCAR3 cells with knock-down expression of (OVCAR3 SUSD2-KD) or endogenous expression of (OVCAR3-Non-Targeting (NT)) were injected into the peritoneal cavity of athymic nude mice. Immunohistochemistry analysis was utilized to identify infiltrating cancer cells and metastatic tumors in mouse ovaries, pancreas, spleen, omentum and liver. OVCAR3-NT mice developed significantly less cancer cell infiltrate and tumors in their pancreas and omentum compared to OVCAR3 SUSD2-KD mice. Furthermore, OVCAR3-NT mice displayed a longer median survival when compared to OVCAR3 SUSD2-KD mice (175 days and 185.5 days, respectively; -value 0.0159). Altogether, the findings generated through the preclinical mouse model suggest that increased expression in HGSOC impedes metastasis to pancreas and omentum. These results correlate to longer median survival and prove to be consistent with previous findings showing prolonged survival of HGSOC patients with high -expressing primary tumors.