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Lasp1 gene disruption is linked to enhanced cell migration and tumor formation

ABSTRACT: Chronic loss of Lasp1 alters the expression of other genes associated with cell motility/attachment, and/or other cellular functions. Results provide new information showing that loss of Lasp1 leads to up- and down-regulation of genes involved in cell motility/attachment/growth. Keywords: Genotype comparison

ORGANISM(S): Mus musculus

PROVIDER: GSE14800 | GEO | 2009/02/12

SECONDARY ACCESSION(S): PRJNA111969

REPOSITORIES: GEO

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Lasp1 gene disruption is linked to enhanced cell migration and tumor formation

Project description:Chronic loss of Lasp1 alters the expression of other genes associated with cell motility/attachment, and/or other cellular functions. Results provide new information showing that loss of Lasp1 leads to up- and down-regulation of genes involved in cell motility/attachment/growth. Keywords: Genotype comparison Total RNA isolated from Lasp1-/- MEFs compared to Lasp1+/+ MEFs.

2010-06-23 | E-GEOD-14800 | biostudies-arrayexpress

Lasp1 gene disruption is linked to enhanced cell migration and tumor formation.

Project description:Lasp1 is an actin-binding, signaling pathway-regulated phosphoprotein that is overexpressed in several cancers. siRNA knockdown in cell lines retards cell migration, suggesting the possibility that Lasp1 upregulation influences cancer metastasis. Herein, we utilized a recently developed gene knockout model to assess the role of Lasp1 in modulating nontransformed cell functions. Wound healing and tumor initiation progressed more rapidly in Lasp1(-/-) mice compared with Lasp1(+/+) controls. Embryonic fibroblasts (MEFs) derived from Lasp1(-/-) mice also migrated more rapidly in vitro. These MEFs characteristically possessed increased focal adhesion numbers and displayed more rapid attachment compared with wild-type MEFs. Differential microarray analyses revealed alterations in message expression for proteins implicated in cell migration, adhesion, and cytoskeletal organization. Notably, the focal adhesion protein, lipoma preferred partner (LPP), a zyxin family member and putative Lasp1 binding protein, was increased about twofold. Because LPP gene disruption reduces cell migration, we hypothesize that LPP plays a role in enhancing the migratory capacity of Lasp1(-/-) MEFs, perhaps by modifying the subcellular localization of other motility-associated proteins. The striking contrast in the functional effects of loss of Lasp1 in innate cells compared with cell lines reveals distinct differences in mechanisms of motility and attachment in these models.

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Lasp1 gene deletion: Effect on gene expression in the gastric mucosa

Project description:Comparative analysis of gene expression in murine gastric fundic mucosa in wild-type and Lasp1-null littermates. The data provide a comprehensive overview of genes expressed in the mouse gastric mucosa and show that the expression of several known and unidentified genes is modified by disruption of the Lasp1 gene. Keywords: Genotypic comparison

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Project description:The process of tumor invasion requires degradation of extracellular matrix by proteolytic enzymes. Cancer cells form protrusive invadopodia, which produce and release matrix metalloproteinases (MMPs) to degrade the basement membrane and thereby allowing metastasis. We investigated the effect of LASP1, a newly identified protein in invadopodia, on expression, secretion and activation of MMPs in invasive breast tumor cells. By analyzing and verifying microarray data sets and performing reporter assays, we demonstrate that LASP1 positively modulates the expression of c-Fos and AP-1 activity, and thereby up-regulates expression of MMP1, -3 and -9 in breast cancer cells. Furthermore, zymography assays and Western blot analysis revealed cytosolic LASP1 promotion of MMP vesicle secretion into the extracellular matrix, thus altering the microenvironment during cancer progression. The newly identified role of LASP1 in regulating matrix degradation by affecting MMP transcription and secretion elucidated the migratory potential observed in studies that investigated the upregulation of LASP1 in aggressive cancers.

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Klf4 gene disruption is linked to enhanced cellular proliferation and tumor formation

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