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

Abstract

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.

• Authors: Lu Yan, Kazuya Tsujita, Yasuyuki Fujita, Toshiki Itoh
• Journal: FEBS letters (FEBS Lett) Vol. 595 Issue 9 Pg. 1303-1312 (05 2021) ISSN: 1873-3468 [Electronic] England
• PMID: 33540467 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2021 Federation of European Biochemical Societies.

Chemical References

• PTEN Phosphohydrolase
• PTEN protein, human
• ras Proteins

Topics

• Animals
• Cell Movement (genetics)
• Cell Transformation, Neoplastic (genetics)
• Dogs
• Epithelial Cells (metabolism, pathology)
• Humans
• Neoplasm Invasiveness (genetics, pathology)
• Neoplasms (genetics, pathology)
• PTEN Phosphohydrolase (genetics)
• Phosphatidylinositol 3-Kinases (genetics)
• ras Proteins (genetics)