PTEN is required for the migration and invasion of Ras-transformed MDCK cells

FEBS Letters

article

Lu Yan¹  Kazuya Tsujita¹  Yasuyuki Fujita³  Toshiki Itoh¹ 

[1] Division of Membrane Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine;Biosignal Research Center, Kobe University;Division of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering;Division of Molecular Oncology, Graduate School of Medicine, Kyoto University

关键词: cancer cell invasion;    PI3K;    PTEN;    Ras;   

DOI  :  10.1002/1873-3468.14053

来源: John Wiley & Sons Ltd.

【 摘 要 】

The balance between phosphoinositides distributed at specific sites in the plasma membrane causes polarized actin polymerization. Oncogenic transformations affect this balance by regulating phosphoinositide 3-kinase (PI3K) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN), causing metastatic behavior in cancer cells. Here, we show that the PTEN tumor suppressor gene is required for epithelial cancer cell invasion. Loss of PTEN in Ras-transformed MDCK cells suppressed their migratory phenotype in collagen gel and invasion through Matrigel. Rescue experiments showed a requirement for the C2 domain-mediated membrane recruitment of PTEN, which is typically observed at the rear side of invading cancer cells. These findings support the role of PTEN in suppression of unwanted leading edges necessary for efficient migration of epithelial cancer cells.

【 授权许可】

Unknown