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Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1
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Document Title
Regulation of Lung Cancer Cell Migration and Invasion by Reactive Oxygen Species and Caveolin-1
Author
Luanpitpong S, Talbott SJ, Rojanasakul Y, Nimmannit U, Pongrakhananon V, Wang LY, Chanvorachote P
Name from Authors Collection
Affiliations
West Virginia University; Chulalongkorn University; Chulalongkorn University; West Virginia University; National Science & Technology Development Agency - Thailand; National Nanotechnology Center (NANOTEC); Centers for Disease Control & Prevention - USA; National Institute for Occupational Safety & Health (NIOSH)
Type
Article
Source Title
JOURNAL OF BIOLOGICAL CHEMISTRY
Year
2010
Volume
285
Issue
50
Page
38832-38840
Open Access
Green Published, hybrid
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI
10.1074/jbc.M110.124958
Format
Abstract
The acquired capability of tumor cells to migrate and invade neighboring tissues is associated with high metastatic potential and advanced stage of cancers. Recently, signaling molecules such as reactive oxygen species (ROS) and caveolin-1 (Cav-1) have been implicated in the aggressive behavior of cancer cells. However, the roles of specific ROS in cancer cell migration and Cav-1 regulation are unclear. We demonstrate here that Cav-1 plays an important role in the migration and invasion of human lung carcinoma H460 cells and that these effects are differentially regulated by cellular ROS. Using various known inhibitors and donors of ROS, we found that different ROS have different effects on Cav-1 expression and cell migration and invasion. Superoxide anion and hydrogen peroxide down-regulated Cav-1 expression and inhibited cell migration and invasion, whereas hydroxyl radical up-regulated the Cav-1 expression and promoted cell migration and invasion. The down-regulating effect of superoxide anion and hydrogen peroxide on Cav-1 is mediated through a transcription-independent mechanism that involves protein degradation via the ubiquitin-proteasome pathway. These results indicate the essential role of different ROS in cancer cell motility and through Cav-1 expression, which may provide a key mechanism controlling tumor progression and metastasis. The upregulation of Cav-1 and cell motility by hydroxyl free radical suggests an important role of this ROS as a positive regulator of tumor progression.
Funding Sponsor
National Institutes of Health [R01-HL076340]; Thailand Research Fund [5.Q.CU/49/A.1]; Ratchadaphiseksomphot Endowment Fund; NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL076340] Funding Source: NIH RePORTER
License
CC BY
Rights
ASBMB
Publication Source
WOS