Ptger3, also known as prostaglandin E receptor 3, is involved in various biological processes. It is part of the prostaglandin E2-prostaglandin E2 receptor EP3 signaling, which is critical for tumor-associated angiogenesis, tumor growth, and chemoresistance. In the body, it participates in regulating cell invasion, migration, and proliferation, and is associated with transmembrane transport-related biological processes [1,2,3].

In triple-negative breast cancer (TNBC), PTGER3 knockdown inhibits the vulnerability of TNBC cells to ferroptosis by increasing GPX4 expression and activating the PI3K-AKT pathway. Upregulation of PTGER3 weakens the epithelial-mesenchymal phenotype in TNBC and promotes ferroptosis both in vitro and in vivo by repressing GPX4 expression [1].

In ovarian cancer, silencing of PTGER3 via siRNA in cancer cells is associated with decreased cell growth, less invasiveness, cell-cycle arrest, and increased apoptosis, mediated through the Ras-MAPK/Erk-ETS1-ELK1/CFTR1 axis [3].

In clear cell renal carcinoma, reduced PTGER3 expression is associated with a poor prognosis and is linked to immune cell infiltration [4].

In conclusion, Ptger3 plays crucial roles in regulating cell behaviors and is significantly associated with the development and progression of multiple cancers including TNBC, ovarian cancer, and clear cell renal carcinoma. The gene knockout and knockdown studies in these cancer models have provided valuable insights into its functions, highlighting Ptger3 as a potential biomarker and therapeutic target for these diseases.