Paper Contents
Abstract
Prostaglandin E2 (PGE2) plays a pivotal role in modulating the tumor microenvironment (TME) and promoting tumorigenesis through complex signaling pathways mediated primarily by EP2 and EP4 receptors. Elevated levels of PGE2, driven by the upregulation of cyclooxygenase-2 (COX-2) in tumors, activate EP2 and EP4 receptors, which are involved in key processes such as cancer cell proliferation, survival, immune suppression, angiogenesis, and metastasis. Through the activation of cAMP, PI3KAKT, and MAPKERK pathways, EP2 and EP4 promote tumor growth by enhancing cell proliferation and inhibiting apoptosis. These receptors also play a crucial role in immune evasion, fostering an immunosuppressive environment by influencing regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), and other immune components. Moreover, PGE2 signaling via EP2 and EP4 contributes to the formation of new blood vessels and facilitates metastasis by promoting epithelial-mesenchymal transition (EMT). Due to their pro-tumorigenic roles, EP2 and EP4 receptors have emerged as promising therapeutic targets. The inhibition of these receptors, either alone or in combination with other treatments such as immune checkpoint blockade, holds potential for enhancing anti-cancer therapies. However, challenges such as resistance mechanisms and identifying suitable biomarkers for patient selection remain critical hurdles in optimizing EP2EP4-targeted interventions.
Copyright
Copyright © 2024 Ms. Mrunal Maruti Karanjkar1. This is an open access article distributed under the Creative Commons Attribution License.
