Increased cell migration and plasticity in Nrf2-deficient cancer cell lines View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-06

AUTHORS

Girish Rachakonda, Konjeti R. Sekhar, Dawit Jowhar, Philip C. Samson, John P. Wikswo, R. Daniel Beauchamp, Pran K. Datta, Michael L. Freeman

ABSTRACT

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression is deregulated in many cancers. Genetic and biochemical approaches coupled with functional assays in cultured cells were used to explore the consequences of Nrf2 repression. Nrf2 suppression by Keap1-directed ubiquitylation or the expression of independent short hairpin RNA (shRNA)/siRNA sequences enhanced cellular levels of reactive oxygen species, Smad-dependent tumor cell motility and growth in soft agar. Loss of Nrf2 was accompanied by concomitant Smad linker region/C-terminus phosphorylation, induction of the E-cadherin transcriptional repressor Slug and suppression of the cell-cell adhesion protein E-cadherin. Ectopic expression of the wildtype but not dominant-negative Nrf2 suppressed the activity of a synthetic transforming growth factor-beta1-responsive CAGA-directed luciferase reporter. shRNA knock-down of Nrf2 enhanced the activity of the synthetic CAGA reporter, as well as the expression of the endogenous Smad target gene plasminogen activator inhibitor-1. Finally, we found that Nrf2/Smad3/Smad4 formed an immunoprecipitable nuclear complex. Thus, loss of Nrf2 increased R-Smad phosphorylation and R-Smad signaling, supporting the hypothesis that loss of Nrf2 in an oncogenic context-dependent manner can enhance cellular plasticity and motility, in part by using transforming growth factor-beta/Smad signaling. More... »

PAGES

3703

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/onc.2010.118

    DOI

    http://dx.doi.org/10.1038/onc.2010.118

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/20440267


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