abstract
Metastasis remains the primary cause of lung cancer. The molecules involved in metastasis may be candidates
for new targets in the therapy of lung cancer. The MEK/ERK signaling pathway has been highlighted
in a number of studies on invasiveness and metastasis. In this paper, we show that the MEK
inhibitor U0126 induces flattened morphology, remodels the actin-based cytoskeleton, and potently
inhibits chemotaxis and Matrigel invasion in the human lung cancer A549 cell line. Furthermore, downregulation
of ERK by small interfering RNA significantly inhibits the invasion of A549 cells and induces
stress fiber formation. Taken together, our findings provide the first evidence that the inhibition of invasion
of lung cancer A549 cells by inhibiting MEK/ERK signaling activity is associated with remodeling of
the actin cytoskeleton, suggesting a novel link between MEK/ERK signaling-mediated cell invasion and
the actin-based cytoskeleton.
abstractMetastasis remains the primary cause of lung cancer. The molecules involved in metastasis may be candidatesfor new targets in the therapy of lung cancer. The MEK/ERK signaling pathway has been highlightedin a number of studies on invasiveness and metastasis. In this paper, we show that the MEKinhibitor U0126 induces flattened morphology, remodels the actin-based cytoskeleton, and potentlyinhibits chemotaxis and Matrigel invasion in the human lung cancer A549 cell line. Furthermore, downregulationof ERK by small interfering RNA significantly inhibits the invasion of A549 cells and inducesstress fiber formation. Taken together, our findings provide the first evidence that the inhibition of invasionof lung cancer A549 cells by inhibiting MEK/ERK signaling activity is associated with remodeling ofthe actin cytoskeleton, suggesting a novel link between MEK/ERK signaling-mediated cell invasion andthe actin-based cytoskeleton.
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