What causes changes in microenvironments associated with PTHrP-produced oral cancer tumors?

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670855
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Surgical dentistry
• Research Institution: Hokkaido University
• Principal Investigator: satoh chiharu 北海道大学, 大学病院, 講師 (50222013)
• Co-Investigator(Kenkyū-buntansha): HIGASHINO FUMIHIRO 北海道大学, 大学院歯学研究科, 准教授 (50301891) ; KITAMURA TETSUYA 北海道大学, 大学院歯学研究科, 助教 (00451451) ; MAISHI NAKO 北海道大学, 遺伝子病制御研究所, 助教 (00632423)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: PTHrP / 腫瘍微小環境 / CAF

Outline of Final Research Achievements

Oral squamous cell carcinoma produce PTHrP, and PTHrP-positive cases showed a statistically significant presence of αSMA positive cancer-associated fibroblasts in the stroma. PTHrP processing was found to exacerbate proliferative activity of fibroblasts, and CAF was obtained, as seen in the expression of αSMA. The fibroblasts expressed PTH1R, a receptor of PTHrP, and PTHrP processing was found to stimulate ERK phosphorylation.
These results suggest that PTHrP produced by oral cancer tumors utilizes ERK activation with PTH/PTHrP as a receptor to induce the fibroblasts in the surrounding microenvironment to develop into CAF.

Free Research Field

口腔外科学