Proliferin-related protein overexpression in SGC‑7901 gastric cancer cells inhibits in vitro cell growth and tumorigenesis in nude mice.

As reported in the literature, the worldwide 5-year overall survival rate for patients with gastric cancer receiving surgical treatment in the progressive stage is less than 25%. Therefore, there is an urgent need for the development of novel therapeutic strategies. Our preliminary studies demonstrated that proliferin-related protein (PRP) inhibits the proliferation of TM3 Leydig testicular cells. To evaluate whether PRP has antitumor effects in vitro and in vivo, we stably expressed PRP in SGC-7901 gastric carcinoma cells. PRP inhibited the proliferation and cell cycle progression of SCG-7901 cells, as determined by cell growth and cell cycle assays. Transwell experiments demonstrated that PRP inhibited the cell migration and invasion of SCG-7901 cells. Western blotting demonstrated that PRP-overexpressing cells had upregulated matrix metalloproteinase 9 (MMP-9) and downregulated tissue inhibitor of metalloproteinases-1 (TIMP-1). In a xenograft tumor formation assay using nude mice, tumors formed by PRP-overexpressing cells had significantly lower weights than those formed by control cells, and the tumor inhibitory rate reached 71.9%. We demonstrated for the first time that PRP inhibits gastric carcinoma cell proliferation, motility, and tumorigenicity in vivo, suggesting that PRP may become an important target for the development of gastric cancer gene therapy.

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