Premium
AFAP‐110 is required for actin stress fiber formation and cell adhesion in MDA‐MB‐231 breast cancer cells
Author(s) -
Dorfleutner Andrea,
Stehlik Christian,
Zhang Jing,
Gallick Gary E.,
Flynn Daniel C.
Publication year - 2007
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21143
Subject(s) - focal adhesion , stress fiber , gene knockdown , microbiology and biotechnology , fibronectin , actin , cell adhesion , cytoskeleton , chemistry , actin cytoskeleton , adhesion , cell , biology , cell culture , signal transduction , biochemistry , extracellular matrix , genetics , organic chemistry
Regulation of actin organization and dynamics is a highly complex process that involves a number of actin‐binding proteins, including capping, branching, severing, sequestering, and cross‐linking proteins. The actin‐binding and cross‐linking protein AFAP‐110 is expressed in normal myoepithelial cells. Screening of different breast epithelial cell lines revealed high expression levels of AFAP‐110 in the human breast cancer cell lines MDA‐MB‐231 and MDA‐MB‐435. Knockdown of AFAP‐110 expression in MDA‐MB‐231 cells does not result in any changes in cell proliferation but did result in a loss of actin stress fiber cross‐linking and decreased adhesion to fibronectin. An inducible knockdown approach confirms that MDA‐MB‐231 breast cancer cells require AFAP‐110 expression for stress fiber formation and adhesion. Thus, AFAP‐110 may provide cytoskeletal tension through stress fiber formation, which is required for focal adhesion formation. Indeed, we could not detect any focal contacts or focal adhesions in AFAP‐110 knockdown cells after adhesion to fibronectin. Although expression levels of crucial focal adhesion components were not influenced by AFAP‐110 expression levels, treatment of AFAP‐110 knockdown cells with LPA did not result in induction of actin stress fibers and focal adhesions. In summary, AFAP‐110 plays an important role in MDA‐MB‐231 breast cancer cell adhesion possibly by regulating stress filament cross‐linking which would promote focal adhesion formation. J. Cell. Physiol. 213:740–749. © 2007 Wiley‐Liss, Inc.