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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 Total RNA isolated from Lasp1-/- MEFs compared to Lasp1+/+ MEFs.

ORGANISM(S): Mus musculus

SUBMITTER: Catherine Chew

PROVIDER: E-GEOD-14800 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Zhang Han H Chen Xunsheng X Bollag Wendy B WB Bollag Roni J RJ Sheehan Daniel J DJ Chew Catherine S CS

Physiological genomics 20090616 3

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. Embryo ...[more]

PMID: 19531578

Similar Datasets

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

2009-02-12 | GSE14800 | GEO

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 Total mRNA isolated from fundic gastric mucosae of three-month old mice, C57Bl/6Ncr strain, was used for this comparison.

2010-06-23 | E-GEOD-14813 | biostudies-arrayexpress

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

Project description:Kruppel-like factor 4 (KLF4) is involved in diverse biological processes such as cell cycle control, differentiation, transcriptional regulation, DNA repair and apoptosis. Furthermore, KLF4 is a tumor suppressor and play a role in regulating genomic stability. In order to investigate the changes in gene expression in the klf4 null MEFs, we compared the gene expression patterns of the wild type and klf4 null by microarray. Total RNA isolated from Klf4 -/- MEFs compared to Klf4 +/+ MEFs. RNA was processed from cells that had reached 80-90 confluency in triplicate using Trizol reagent as recommended by the manufacturer (Invitrogen, Carlsbad, CA). RNA was subjected to DNase I treatment in order to remove any contaminating genomic DNA. Final purification was performed on RNAeasy columns (Qiagen, Valencia, CA), according to the manufacturer's recommendations.

2010-11-25 | E-GEOD-21768 | biostudies-arrayexpress

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

2010-11-25 | GSE21768 | GEO

Characterization of Two Outer Membrane Proteins, FlgO and FlgP, that Influence Vibrio cholerae Motility

Project description:Vibrio cholerae is highly motile by the action of a single polar flagellum. The loss of motility reduces the infectivity of V. cholerae, demonstrating that motility is an important virulence factor. FlrC is the sigma-54-dependent positive regulator of flagellar genes. Recently, the genes VC2206 (flgP) and VC2207 (flgO) were identified as being regulated by FlrC by microarray analysis of an flrC mutant. FlgP is reported to be an outer membrane lipoprotein required for motility that functions as a colonization factor. The study reported here focuses on the characterization of flgO, the first gene in the flgOP operon. We show FlgO/P are important for motility, as these mutants have reduced motility phenotypes. The flgO/P mutant populations display fewer motile cells as well as reduced numbers of flagellated cells. The flagella produced by the flgO/P mutant strains are shorter in length than the WT flagella, which can be restored by inhibiting rotation of the flagellum. FlgO is an outer membrane protein that localizes throughout the membrane and not at the flagellar pole. Although FlgO/P do not specifically localize to the flagellum, they are required for flagellar stability. Due to the nature of these motility defects, we established that the flagellum is not sufficient for adherence, rather, motility is the essential factor required for attachment and thus colonization by V. cholerae O1 of the classical biotype. This study reveals a novel mechanism for which the OMPs FlgO and FlgP function in motility to mediate flagellar stability and influence attachment and colonization. Vibrio cholerae O395 vs. rpoN mutant

2010-05-16 | E-GEOD-17144 | biostudies-arrayexpress

Comparison of gene expression data between control and tissue specific epicardial PDGF receptor (a and b) knockout embryonic hearts

Project description:Epicardial cells undergo an epithelial-to-mesenchymal transtion (EMT) to generate coronary vascular smooth muscle cells (VSMC) and cardiac fibroblasts. Little is known about the mechanisms regulating EMT or the in vivo signals directing epicardial-derived cell (EPDC) fate. Here, we show that loss of PDGF signaling leads to a disruption in Sox9 expression, and when Sox9 expression was restored in mutant hearts, the EMT defect was rescued. Interestingly, mutants lacking only one of the PDGF genes exhibited a lineage specific requirement for the individual receptors. Loss of PDGFRα resulted in a deficit in cardiac fibroblast formation, while cVSMC development was unperturbed. Conversely, PDGFRβ was required for cVSMC development but not cardiac fibroblast development. Combined, our data demonstrate a novel role for PDGF receptors in epicardial EMT and EPDC development. GSM671723-GSM671724: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout hearts using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA) GSM671877-GSM671882: Total RNA was isolated from E12.5 control and PDGF receptor epicardial knockout primary epicardial cultures using the Trizol reagent. RNA was processed as per manufacturer's instructions (Illumina Gene expression array, Illumina, inc. San Diego, CA, USA)

2011-02-28 | E-GEOD-27181 | biostudies-arrayexpress

Characterization of Two Outer Membrane Proteins, FlgO and FlgP, that Influence Vibrio cholerae Motility

2009-07-18 | GSE17144 | GEO

Loss of MBNL Leads to Disruption of Developmentally Regulated Alternative Polyadenylation in RNA-Mediated Disease

Project description:Mapping MBNL-regulated genome-wide alternative polyadenylation: We report that depletion of Mbnl proteins in mouse embryo fibroblasts (MEFs), DM mouse model quadriceps muscle, and DM-autopsy muscle tissue leads to mis-regulation of alternative polyadenylation We compared WT, Mbnl1/2KO, Mbnl1/2KO/3siRNA, and Mbnl1/2KO/scrambled siRNA MEFs (n=2 for each group) to evaluate alternative polyadenylation shifts that occur due to progressive loss of Mbnl proteins. We also compared WT (1 day old, and 4 months old, n=2 each) and HSALR mouse model (4 months old, n=2) of myotonic dystrophy for developmental alternative polyadenylation defects in myotonic dystrophy. Finally, we compared control and DM1 autopsy muscle tissues (n=3) for changes in alternative polyadenylation. We performed HITS-CLIP analysis of binding sites of Mbnl1, Mbnl2 and Mbnl3 in MEFs (n=3 each). We also performed HITS-CLIP analysis for major skeletal muscle Mbnl protein, Mbnl1 in FVB WT adult muscle (4 months, n=3). Finally we performed HITS-CLIP analysis for CPSF6 in WT and Mbnl1/2 KO MEFs (n=3 each) Please note that the 'readme_Table.txt' describes the contents of 'Table S*.xlsx' files, and the readme_method.txt include additional details about experiemenal procedures.

2014-09-05 | E-GEOD-60487 | biostudies-arrayexpress

Regulation of matrix metalloproteinases (MMPs) expression and secretion by LIM and SH3 protein (LASP1)

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.

2017-02-03 | GSE77584 | GEO

Disruption of Multiple Overlapping Functions Following Step-Wise Inactivation of the Extended Myc Network

Project description:Myc, a member of the Myc Network, supervises proliferation, metabolism and ribosomal function. The Mlx Network cross-talks with the Myc Network and regulates overlapping functions. We describe here the consequences of conditional Myc and/or Mlx gene knockouts (KOs) in primary and immortalized murine embryonic fibroblasts (MEFs). MycKO and MycKOxMlxKO “double KO” (DKO) primary MEFs, but not MlxKO MEFs, rapidly growth-arrested and displayed features of aging and senescence. In DKO MEFs, these were transient, indicating that Mlx was necessary to maintain them. KO MEFs deregulated transcripts pertaining to mitochondrial and ribosomal structure and function, cell cycle, aging, senescence and DNA damage. The expression of DNA damage-related proteins was also abnormal. Immortalized KO MEFs remained proliferation-competent but demonstrated differential sensitivities to genotoxic agents. Immortalized MycKO MEFs spontaneously developed tetraploidy that was Mlx-dependent. Different aspects of MEF aging, senescence and DNA damage responses are therefore differentially regulated by the Myc and Mlx Networks.

2023-08-28 | GSE210362 | GEO

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