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Articles in PresS, published online ahead of print November 30, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00291.2001
Submitted on July 28, 2001
Accepted on November 14, 2001
1 Pulmonary/Medicine, University of Pennsylvania, Philadelphia, PA, USA
2 MD Anderseon Cancer Center, University of Texas, Smithville, TX, USA
* To whom correspondence should be addressed. E-mail: krymskay{at}mail.med.upenn.edu.
The loss of function of the tumor suppressor gene TSC2 and its protein product, tuberin, promotes the development of benign lesions by stimulating cell growth; although, the role of tuberin in regulating cell migration and metastasis has not been characterized. In addition, the role of PI3K activity, an important signaling event regulating cell migration, in modulating tuberin-deficient cell motility remains unknown. Using a tuberin-deficient rat smooth muscle cell line, ELT3, we demonstrate that PDGF stimulates cell migration by 3.2-fold, while VEGF, TGF
, and bFGF increase migration by 2.1-, 2.1- and 2.6-fold, respectively. Interestingly, basal and PDGF-induced migration in tuberin-deficient ELT3, ELT4, and ERC15 cells were not significantly different from that of tuberin-positive TRKE2, ASM and PAVSM cells. Expression of tuberin in tuberin-deficient ELT3 cells also had little effect on cell migration. In parallel experiments, the role of PI3K activation in cell migration was investigated. LY294002, a PI3K inhibitor, decreased PDGF-induced migration in a concentration-dependent manner with an IC50 of about 5 µM. LY294002 also abrogated ELT3 cell migration stimulated by bFGF-, and TGF, but not by VEGF and PMA. Further, transient expression of constitutively active PI3K (p110*) was sufficient to induce ELT3 cell migration. However, the migration induced by p110* was less than that induced by growth factors suggesting other signaling pathways are also critically important in modulating growth factor-induced cell migration. These data suggest that PI3K is required for growth factor-induced cell migration and loss of tuberin appears to have little effect on cell migration.
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