Clinical Detection And Mechanism Of S100P In Endometrial Cancer

Purpose:S100P was reported to be involved in the genesis, migration of multiple cancers, affecting their prognosis and drug resistance. However, little was known about the expression manner and functional role of S100P in endometrial cancer. In the current study we assessed the expression of S100P in surgically resected endometrial cancer specimens, and further demonstrated the functional significance and mechanism of S100P in vitro endometrial cancer cells by in vitro transfection model.Materials and methods:Endometrial carcinoma tissues were collected from12patients who underwent surgical resection from2000to2010. Expression of S100P level in these specimens was assessed by immunohistochemistry. Full-length human S100P cDNA was cloned into PLVX-puro vector. HEC-1A cells were selected as cell models for S100P cDNA transfection. Cell biologic features including cell proliferation, apoptosis, cell cycle, drug resistance, invasion and migration, potential signal transduction pathways was observed after successful transfection.Results:significantly elevated expression of S100P was detected in all the5cases of Squamous cell carcinoma of the endometrium (100%). However, S100P expression in7 endometrial adenocarcinoma samples was relatively much lower. After transfection.S100P expression in HEC-1A cell was significantly elevated both in mRNA levels and protein levels. Up regulation of SI OOP promoted proliferation, survival, invasion and migration while reduced apoptosis of HEC-1A cell. Elevated levels of S100P were related to drug-resistance in endometrial cancer cells to cisplatin (CDDP). This study also revealed that significance differences of cell cycle phase had been changed by transfection with S100P cDNA; elevated levels of S100P increased cells in the G1phase of cell cycle while number of cells in the S phase was lower than control group. Some potential signal transduction pathways was observed, higher expression of S100P resulted in the up-regulation of p-ERK, p-JNK, p-AKT, p-PI3K, NF-KB, RAGE, P38(p-MAPK), BCL-XL, and down-regulation of (3-catanin,p53.Conclusion:The expression pattern of S100P was strongly dependent on the histological type of endometrial cancer; through multiple molecular pathways, elevated S100P promoted HEC-1A cell proliferation, migration and invasion, protected cell from natural or CDDP induced cell apoptosis. Our findings indicated that expression of S100P could serve as new clinical and histological diagnostic marker, prognosis indicator and potential therapeutic target of endometrial cancer.