Role of COX-2/PGE2 Mediated Inflammation in Oral Squamous Cell Carcinoma

Abstract

A significant amount of research indicates that the cyclooxygenase/prostaglandin E2 (PGE2) pathway of inflammation contributes to the development and progression of a variety of cancers, including squamous cell carcinoma of the oral cavity and oropharynx (OSCC). Although there have been promising results from studies examining the utility of anti-inflammatory drugs in the treatment of OSCC, this strategy has been met with only variable success and these drugs are also associated with toxicities that make them inappropriate for some OSCC patients. Improved inflammation-targeting therapies require continued study of the mechanisms linking inflammation and progression of OSCC. In this review, a synopsis of OSCC biology will be provided, and recent insights into inflammation related mechanisms of OSCC pathobiology will be discussed. The roles of prostaglandin E2 and cluster of differentiation factor 147 (CD147) will be presented, and evidence for their interactions in OSCC will be explored. Through continued investigation into the protumourigenic pathways of OSCC, more treatment modalities targeting inflammation-related pathways can be designed with the hope of slowing tumour progression and improving patient prognosis in patients with this aggressive form of cancer.

Prostanoid receptor genes confer poor prognosis in head and neck squamous cell carcinoma via epigenetic inactivation

“…Numerous epidemiological studies have shown that the regular intake of the NSAID aspirin, an inhibitor of COXs, substantially reduces both the incidence and progression of several prevalent cancers [20]. Abundant epidemiological and preclinical/clinical studies have demonstrated that celecoxib, a specific COX-2 inhibitor, is related to the suppression of cancer cell proliferation and a decrease in cancer incidence [21]. COX-1 is constitutively expressed in many tissues and regulates basal levels of prostaglandins [22].…”

Combination of β2-AR Blocker and COX-2 Inhibitor Suppresses Development of Oral Squamous Cell Carcinoma

“…reported that cetuximab could suppress the proliferation of cancer cells by inhibiting COX-2/PGE2/EGFR pathway [23]. But the molecular mechanism of β2-AR regulates the expression of EGFR has not been determined.…”

“…Cyclooxygenase-2 (COX-2) is overexpressed and closely related the poor prognosis and progression of malignant tumor, including OSCC [18][19][20][21]. Just like β2-AR, COX-2 is closely related to proliferation, apoptosis, angiogenesis, invasion, metastasis and immunosuppression of OSCC [22,23]. Different studies reported that COX-2 inhibitor could signi cantly inhibit progression of OSCC [24][25][26][27].…”

Peer Review #1 of "Exosomal cargoes in OSCC: current findings and potential functions (v0.1)"

“…Exosomes with high concentrations of prostaglandins transport more PGE2 to neighboring cells, enhancing the overall presence of PGE2 in the microenvironment (Subra et al 2010). Cell motility and metastatic status are impacted by extracellular levels of PGE2 (Nasry et al 2018). Evidence has shown that exosomes rich in PGE2 participate in tumor immune evasion and promote tumor growth (Record et al 2014).…”