The actin cytoskeleton in normal and pathological cell motility

Lambrechts, Anja; Troys, Marleen Van; Ampè, Christophe

doi:10.1016/j.biocel.2004.01.024

Cited by 204 publications

(162 citation statements)

References 148 publications

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“…There is a precedent from the previous studies showing that atypical protein kinase C is involved in the polarized migration of cultured astrocytes (Etienne-Manneville et al, 2005) and that PKCi is involved in the nicotine-activated migration and invasion of H1299 human non-small cell lung cancer cells (Xu and Deng, 2006). The actin cytoskeleton is a dynamic element within cells that undergoes changes that are essential to cell motility (Lambrechts et al, 2004). PKCi depletion resulted in the formation of long actin stress fibers; similar changes in stress fibers were described by Soloff et al (2004), in PKCi knockout mouse embryonic fibroblasts) and other studies have also implicated the atypical protein kinase C family in stress fiber loss (Uberall et al, 1999;Coghlan et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Regulation of glioblastoma cell invasion by PKCι and RhoB

Baldwin

Parolin²,

Lorimer

2008

Oncogene

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Section: Discussionmentioning

confidence: 99%

Regulation of glioblastoma cell invasion by PKCι and RhoB

Baldwin

Parolin²,

Lorimer

2008

Oncogene

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“…Although actin concentrations in general appear unaltered, F-actin-stained filopodia extending about the periphery of the cells was reduced by 1000 mM BA. With actin serving an important cytoskeletal factor in cell migration and invasion (Lambrechts et al, 2004), the observed F-actin retraction in BA-treated cells suggests a reduced capacity to perform either. This interpretation was reinforced by the analysis showing a dose-dependent inhibitory effect on motility and invasion capacity, along with incompetence for reattachment ( Figure 3B and C).…”

Section: Morphologymentioning

confidence: 99%

Cellular changes in boric acid-treated DU-145 prostate cancer cells

Barranco

Eckhert

2006

Br J Cancer

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Epidemiological, animal, and cell culture studies have identified boron as a chemopreventative agent in prostate cancer. The present objective was to identify boron-induced changes in the DU-145 human prostate cancer cell line. We show that prolonged exposure to pharmacologically-relevant levels of boric acid, the naturally occurring form of boron circulating in human plasma, induces the following morphological changes in cells: increases in granularity and intracellular vesicle content, enhanced cell spreading and decreased cell volume. Documented increases in b-galactosidase activity suggest that boric acid induces conversion to a senescentlike cellular phenotype. Boric acid also causes a dose-dependent reduction in cyclins A -E, as well as MAPK proteins, suggesting their contribution to proliferative inhibition. Furthermore, treated cells display reduced adhesion, migration and invasion potential, along with F-actin changes indicative of reduced metastatic potential. Finally, the observation of media acidosis in treated cells correlated with an accumulation of lysosome-associated membrane protein type 2 (LAMP-2)-negative acidic compartments. The challenge of future studies will be to identify the underlying mechanism responsible for the observed cellular responses to this natural blood constituent.

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“…Another protein, p34-Arc is one of seven subunits of the Arp2/3 complex that is strongly concentrated in the earliest aggregation of F-actin formed in response to growth factors [23], and that creates Y-shaped junctions on existing filaments resulting in branched actin networks [24,25]. Nucleation-promoting factors like the Wiskott-Aldrich syndrome protein (WASP) family integrate multiple upstream signals to induce actin polymerization through the Arp2/3 complex, which increases the cell protrusive activity associated with cell migration and invasion [24,25].…”

Section: Actin Remodeling Proteins Are Upregulated In Cancer Tissuesmentioning

confidence: 99%

Proteomic analysis of breast cancer tissue reveals upregulation of actin‐remodeling proteins and its relevance to cancer invasiveness

Kim

Bae

Lee

et al. 2009

Proteomics Clinical Apps

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There is an emerging interest in protein expression profiling with the aim of identifying novel diagnostic markers and therapeutic targets in breast cancer. We analyzed breast cancer tissues by 2-D DIGE using a narrow range IPG strip (pH 5.5-6.7) after the immunodepletion of serum albumin and Ig. Sixty-three protein spots were detected with more than 61.8-fold differences (p ,0.05 for three technical replicates) from a set of tissue samples in which three tumor and three nontumor samples were randomly selected from six breast cancer subjects and pooled separately. Of these, 53 proteins were successfully identified by MS. Among the proteins whose levels were increased, we identified three novel WD-repeat-motifbearing proteins that have been known to be involved in actin remodeling: Arp2/3 complex subunit 2 (p34-Arc), coronin-1A and WD-repeat protein 1 (Wdr1). Significantly increased amounts of p34-Arc and coronin-1A in breast cancer were also shown by Western blot analysis of matched tumor and nontumor tissue samples (N = 11, p ,0.05), and were consistent with the mRNA levels retrieved from publicly available microarray databases. The siRNA knockdown of p34-Arc attenuated the invasion of SK-BR3 breast cancer cells into Matrigel. In contrast, the overexpression of coronin-1A increased this invasive activity. Taken together, the cellular levels of p34-Arc and coronin-1A were linked to cancer development and migration. The data obtained from the present study provides new insight into the management of breast cancer.

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The actin cytoskeleton in normal and pathological cell motility

Cited by 204 publications

References 148 publications

Regulation of glioblastoma cell invasion by PKCι and RhoB

Regulation of glioblastoma cell invasion by PKCι and RhoB

Cellular changes in boric acid-treated DU-145 prostate cancer cells

Proteomic analysis of breast cancer tissue reveals upregulation of actin‐remodeling proteins and its relevance to cancer invasiveness

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