Function of PRL-3 in oral squamous cell carcinoma

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K20579
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• Research Institution: Okayama University
• Principal Investigator: Yoshida Shoko 岡山大学, 大学病院, 医員 (00616047)
• Research Collaborator: SASAKI Akira 岡山大学, 大学院医歯薬学総合研究科, 教授 (00170663) ; SHIMO Tsuyoshi 北海道医療大学, 歯学部, 教授 (40362991) ; KISHIMOTO Koji 岡山大学, 大学院医歯薬学総合研究科, 助教 (40243480) ; MURASE Yurika 岡山大学, 大学病院, 医員 (70803708)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: PRL-3 / 口腔扁平上皮癌 / 浸潤

Outline of Final Research Achievements

This study assessed the function of PRL-3 in the progression of oral squamous cell carcinoma. In human oral squamous cell carcinoma cell lines, PRL-3 showed an expression pattern similar to that of E-cadherin which disappears in the course of epithelial-mesenchymal transition (EMT). E-cadherin was also highly expressed in the most invasive part of the oral squamous cell carcinoma tissue in which PRL-3 is highly expressed. In addition, the expression of PRL-3 was low in gingival squamous cell carcinoma tissues with jaw bone invasion. On the contrary, PRL-3 and E-cadherin were both highly expressed in the gingival squamous cell carcinoma tissue without the jaw bone invasion. These results demonstrated that PRL-3 has a function of suppressing EMT via E-cadherin and suppress the invasion of oral squamous cell carcinoma.

Free Research Field

外科系歯学

Academic Significance and Societal Importance of the Research Achievements

学術的意義：本研究から、PRL-3はE-cadherinを介してEMTを抑制し、口腔扁平上皮癌の浸潤を抑制する可能性が推察された。また、PRL-3は顎骨浸潤も抑制する可能性が示唆された。
社会的意義：本研究から、PRL-3が口腔扁平上皮癌の浸潤の早期診断マーカーになることが期待でき、PRL-3を分子標的とした浸潤抑制薬開発への貢献が期待できる。