High Glucose Stimulates Inflammation by Increasing the Expression and Function of Fpr1 in Endometrial Cancer

Endometrial cancer is one of the most fast-rising malignancies and tending to be young onset in Taiwan population. Many factors are considered as risk factors for endometrial cancer such as obesity-related comorbidities including diabetes and metabolic syndrome. N-formyl peptide receptor 1 (FPR1) is involved in inflammation, cancer, and infection. Overexpressed FPR1 is associated with tumor progression in various cancers. Moreover, accumulating evidence demonstrates that FPR1 contributes to tumor progression by mediating tumor cell proliferation via promoting inflammation. Our team collaborator has reviewed FPR1-related inflammatory processes. However, the role of FPR1 in tumorigenesis of endometrial cancer remains unclear. The aim of this study is to investigate whether high glucose stimulates inflammation by increasing the expression and function of FPR1 in endometrial cancer. Specifically, (1) to investigate high glucose-induced inflammation in endometrial cancer; (2) to determine the correlation between FPR1 expression and cancer cells viability along with female mice model; (3) to analyze the association between FPR1 and neutrophil to lymphocyte ratio (NLR) in diabetic and non-diabetic patients with endometrial cancer, and whether FPR1 is a prognostic factor in endometrial cancer.The findings of this study will provide information on the mechanism of how high glucose stimulates the proliferation of human endometrial cancer cells via inflammation by FPR1. Clinical implication of FPR1 combining NLR may become potential markers for the diagnosis and monitoring of patients with endometrial cancer. Targeting FPR1 activity may thus have potential roles in the management of endometrial cancer patients.

Project ID:PF10907-2414
External Project ID:MOST109-2629-B182A-002