Survival mechanism of CD271-positive HNSCC and itstherapeutic intervention

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K20238
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Otorhinolaryngology
• Research Institution: Miyagi Prefectural Hospital Organization Miyagi Cancer Center
• Principal Investigator: IMAI TAKAYUKI 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 特任研究員 (80408583)
• Co-Investigator(Renkei-kenkyūsha): MATSUURA Kazuto 地方独立法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 特任研究員 (70271947)
• Research Collaborator: TANAKA Nobuyuki 地方独立法人宮城県立病院機構宮城県立がんセンター(研究所), がん先進治療開発研究部, 部長 (60280872)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: CD271 / 頭頸部癌

Outline of Final Research Achievements

To determine a potential role of CD271 in a squamous cell carcinoma, CD271 was knock-downed by shRNA. CD271 mRNA knockdown inhibited both cell proliferation and migration. p42/44Erk inhibition as well as RhoA inhibition ameliorated the malignant phenotypes of hypopharyngeal HPCM2 cells. An anti-CD271 Ab, however, did not show a significant in vitro effect on the cells. Taken together, CD271 is shown to be a potential target for squamous cell carcinoma therapy.

Free Research Field

頭頸部外科学