Is sphingolipid of the cell membrane involved in invasion and metastasis of adenocarcinoma of the lung?

2016 Fiscal Year Final Research Report

• Project/Area Number: 26460442
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Human pathology
• Research Institution: Kanazawa Medical University
• Principal Investigator: UEDA Yoshimichi 金沢医科大学, 医学部, 教授 (50271375)
• Co-Investigator(Renkei-kenkyūsha): OKAZAKI Toshirou 金沢医科大学, 医学部, 教授 (40233308)
• Research Collaborator: SHIMASAKI Miyako 金沢医科大学, 医学部, 助教 (00440511)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 細胞膜スフィンゴ脂質 / 肺腺癌 / 浸潤・転移 / Sphingosin kinase 1 / Sphingosine-1-p受容体 / Sphyngomyelinase / 細胞移動

Outline of Final Research Achievements

Investigation aimed at elucidating the involvement of sphingolipid, particularly sphingosin-1 phosphate and sphyngomyelin, in the aggresiveness of non-small cell lung cancer (NSCLC) revealed the following results: 1) Sphingosin kinase (SpK)-1 was expressed in the tumor cells at the front of invasion of NSCLC and micropapillary adenocarcinoma as well as bronchioloalveolar carcinoma cells. 2) Expression of SpK-1 correlated with that of not proliferation-related but ofEMA-related molecules. 2) S1P receprot-2 was localized in the cell membrane of tumor cells at the invasion front. 3) Inhibition of SMS-1, SMS-2 or both gene by siRNA decreased cell motility and invasiveness of HT1080 cells.
These results suggest the pivotal role of cell membranous sphingolipid, particularly sphingosine and sphingomyelin in the invasiveness of NSCLC cells. Further study is warranted to establish a novel therapy against intractable advanced NSCLC from the view of cell membranous sphingolipid.

Free Research Field

人体病理