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Copyright (c) 2024 Young-Rak Cho, Eun-Kyung Ahn, Kyu-Bong Kim, Choong-Hyun Lee, Yoon Gyoon Kim, Joa Sub Oh, Dong-Wan Seo
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Reduction in integrin a3b1 modulates lung cancer motility and invasion through p70S6K-dependent E-cadherin localization
Corresponding Author(s) : Dong-Wan Seo
Cellular and Molecular Biology,
Vol. 70 No. 11: Issue 11
Abstract
In the current study, we investigated the effects and action mechanism of integrin a3b1 in modulating non-small cell lung cancer (NSCLC) growth and progression. Reduced expression of integrin a3 by RNA silencing in p53 wild-type A549 NSCLC cells inhibits cell migration and invasion, compared with those in control cells. These anti-migratory and anti-invasive properties in integrin a3-silenced cells were associated with epithelial cadherin (E-cadherin) distribution at cell-cell contacts, and these effects require the activation of p70 S6 kinase (p70S6K) as evidenced by treatment with rapamycin. Disruption of E-cadherin or blockade of p70S6K activation abrogated the ability of integrin a3-silencing to inhibit cell migration and invasion. In contrast, enhanced proliferation in integrin a3-silenced cells was not affected by the changes in E-cadherin expression. These findings demonstrate the ability of integrin a3b1 to differentially regulate NSCLC cell growth and progression depending on the p53 status, and suggest that integrin a3b1-p70S6K-p53 network may be a promising target for the treatment of NSCLC.
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