Literature DB >> 16309239

Adenovirus-mediated transfer of FRNK augments drug-induced cytotoxicity in cultured SCCHN cells.

Lori J Kornberg1.   

Abstract

BACKGROUND: Focal adhesion kinase (FAK), which is overexpressed in many human epithelial cancers, regulates cell cycle progression, cellular migration, invasion and survival.
MATERIALS AND METHODS: In order to determine if inhibiting FAK activity augments drug-induced cytotoxicity in transformed epithelial cells from the head and neck region (SCCHN cells), cells were transfected with a recombinant adenovirus causing overexpression of FRNK a dominant negative inhibitor of FAK
Results: When SCCHN cells (SCC25 and RPMI 2650) were transfected with Ad-FRNK there was a decrease in autophosphorylation of FAK, coincident with a large increase in FRNK expression. Ad-FRNK and cytotoxic drugs were more effective in reducing cell viability and increasing apoptosis then Ad-FRNK alone or drugs alone. Transfection with Ad-FRNK also led to substantially decreased migration of cultured SCCHN cells. These results indicate that FAK may be a good target for anticancer therapy.

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Year:  2005        PMID: 16309239

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  3 in total

1.  Adenoviruses increase endothelial cell proliferation, migration, and tube formation: partial reversal by the focal adhesion kinase inhibitor, FRNK.

Authors:  Lori J Kornberg; Maria B Grant
Journal:  Microvasc Res       Date:  2007-02-23       Impact factor: 3.514

Review 2.  Focal adhesion kinase as a cancer therapy target.

Authors:  Vita M Golubovskaya
Journal:  Anticancer Agents Med Chem       Date:  2010-12       Impact factor: 2.505

3.  The dual kinase complex FAK-Src as a promising therapeutic target in cancer.

Authors:  Victoria Bolós; Joan Manuel Gasent; Sara López-Tarruella; Enrique Grande
Journal:  Onco Targets Ther       Date:  2010-06-24       Impact factor: 4.147

  3 in total

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