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Selective EP2 and Cox-2 inhibition suppresses cell migration by reversing epithelial-to-mesenchymal transition and Cox-2 overexpression and E-cadherin downregulation are implicated in neck metastasis of hypopharyngeal cancer.

Yoshihiro Watanabe, Yorihisa Imanishi, Hiroyuki Ozawa, Koji Sakamoto, Ryoichi Fujii, Seiji Shigetomi, Noboru Habu, Kuninori Otsuka, Yoichiro Sato, Mariko Sekimizu, Fumihiro Ito, Yuichi Ikari, Shin Saito, Kaori Kameyama, Kaoru Ogawa

2020PubMed23 citationsOpen Access PDF

Abstract

. Multivariate logistic regression revealed that overexpression of Cox-2 (P < 0.001) and downregulation of E-cadherin (P = 0.016) were both independently predictive of neck metastasis. These results suggest that suppression of cell migration ability via reversing EMT by inhibiting the Cox-2/EP2 signaling may contribute to preventing the development and progression of lymphatic metastasis. Collectively, targeting Cox-2/EP2, especially using EP2 antagonist, can be a promising therapeutic strategy by exerting an anti-metastatic effect via EMT reversal for improving the treatment outcomes of patients with various cancers including HPSCC.

Topics & Concepts

Prostaglandin E2 receptorEpithelial–mesenchymal transitionCancer researchDownregulation and upregulationVimentinMetastasisCell migrationCancerMedicineCellReceptorInternal medicineChemistryImmunohistochemistryGeneAgonistBiochemistryInflammatory mediators and NSAID effectsEstrogen and related hormone effectsCancer, Stress, Anesthesia, and Immune Response
Selective EP2 and Cox-2 inhibition suppresses cell migration by reversing epithelial-to-mesenchymal transition and Cox-2 overexpression and E-cadherin downregulation are implicated in neck metastasis of hypopharyngeal cancer. | Litcius