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Quantitative real-time RT-PCR analysis of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector control.

ABSTRACT: The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42587 | GEO | 2013/07/30

SECONDARY ACCESSION(S): PRJNA182321

REPOSITORIES: GEO

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Quantitative real-time RT-PCR analysis of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector control.

Project description:The protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. Studies have shown a relationship between PRL-1 and the expression or activity levels of various molecules involved in integrin-mediated cell signaling. These integrin-responsive players can promote re-arrangements in the actin cytoskeleton that are central to cell motility, invasion, and metastasis. Therefore, to investigate the effects of PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells, we used qRT-PCR to examine the expression levels of 184 genes which either were identified by microarray and proteomic analysis to be differentially expressed in response to PRL-1 or have known associations to integrin-mediated signaling, cytoskeletal remodeling, and/or cell motility. Total RNA was extracted from duplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were analyzed using custom TaqMan Array 96-well Plates to examine the expression of 184 genes with known involvement in or association with signaling pathways related to integrin-mediated cell adhesion, cytoskeletal remodeling, and/or cell motility.

2013-07-30 | E-GEOD-42587 | biostudies-arrayexpress

Expression profile of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector (control)

2013-07-30 | GSE42586 | GEO

Expression profile of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector (control)

Project description:The multifunctional protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. We used Affymetrix Human Genome U133 Plus 2.0 arrays to examine the global molecular changes of gene expression occurring in response to stable PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells. Total RNA was extracted from triplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were hybridized to Affymetrix HG U133 Plus 2.0 microarrays (1 array per sample for a total of 6 arrays). One of the arrays hybridized with a PRL-1 transfected sample was excluded after qRT-PCR demonstrated that this sample did not exhibit increased PRL-1 expression over the level of the empty vector controls. The remaining 2 HEK293-PRL-1 samples both expressed PRL-1 at least 2-fold higher than any of the 3 empty vector controls.

2013-07-30 | E-GEOD-42586 | biostudies-arrayexpress

Comparison of gene expression profiles of neonate rat cardiomyocytes (NRCMs) transfected with LacZ, 23k prolactin (PRL), or 16k PRL.

Project description:Recently, it is reported that multiple signaling pathways are involved with the pathogenesis of PPCM. Here, we show that 23k PRL activates PERK signaling.

2021-04-30 | GSE169063 | GEO

PRL-1 selectively dephosphorylates TIMELESS

Project description:The timing of behavior under natural light-dark conditions is a function of circadian clocks and photic input pathways. Yet a mechanistic understanding of how these pathways collaborate in animals is lacking. Here we demonstrate in Drosophila that the Phosphatase of Regenerating Liver-1 (PRL-1) sets period length and behavioral phase gated by photic signals. PRL-1 knockdown in PDF clock neurons dramatically lengthens circadian period. PRL-1 mutants exhibit allele-specific interactions with the light- and clock-regulated gene timeless (tim). Moreover, we show that PRL-1 promotes TIM accumulation and dephosphorylation. Interestingly, the PRL-1 mutant period lengthening is suppressed in constant light and PRL-1 mutants display a delayed phase under short, but not long, photoperiod conditions. Thus, our studies reveal that PRL-1 dependent dephosphorylation of TIM is a core mechanism of the clock that sets period length and phase in darkness, enabling the behavioral adjustment to changing day-night cycles.

2020-11-11 | PXD020986 | Pride

Microarray analysis of multiple myeloma cell line INA-6 overexpressing PRL-3 vs. Mock control cells

Project description:PRL-3 is an oncogenic phosphatase, which is expressed at a higher level in malignant plasma cells from multiple myeloma patients than in plasma cells from healthy donors and high expression is associated with a poor prognosis. We overexpressed PRL-3 in a multiple myeloma cell line and our goal was to find signaling pathways regulated by PRL-3 in myeloma cells.

2021-07-01 | E-MTAB-10436 | biostudies-arrayexpress

Investigation of the role of PRL-3 in leukemogenesis

Project description:In order to investigate the role of PRL-3 in the leukemogenesis, we transfected a control vector (pEGFP) and (human) PRL-3 gene into an acute myeloid leukemia (AML) cell line TF-1, respectively. After drug selection and FACS sorting, we established TF1-pEGFP and TF1-hPRL-3 isogenic cell lines. In vitro and in vivo experiments were conducted to characterized this pair of isogenic cell lines. Results provided insight into the molecular basis of PRL-3 in contributing the development of AML.

2017-01-11 | GSE64872 | GEO

Blocking the Angiopoietin-2-dependent Integrin beta-1 signaling axis abrogates small cell lung cancer invasion and metastasis

Project description:Small cell lung cancer (SCLC) is the most aggressive lung cancer entity with an extremely limited therapeutic outcome. Most patients are diagnosed at an extensive stage. However, the molecular mechanisms driving SCLC invasion and metastasis remain largely elusive. We used an autochthonous SCLC mouse model and matched primary and metastatic SCLC patient samples to investigate the molecular characteristics of tumor metastasis. We demonstrate that tumor cell invasion and liver metastasis in SCLC are triggered by an Angiopoietin-2/Integrin beta-1-dependent pathway in tumor cells, mediated by focal adhesion kinase-Src kinase signaling. Strikingly, CRISPR-Cas9 knock out of Integrin beta-1 or blocking Integrin beta-1 signaling by an anti-Angiopoietin-2 treatment abrogates liver metastasis formation in vivo. Interestingly, analysis of a unique collection of matched primary and metastatic SCLC patient samples confirmed a strong increase of Integrin beta-1 in liver metastasis in comparison to the primary tumor. We further show that Angiopoietin-2 blockade combined with anti-VEGFR and PD-1-targeted treatment displays synergistic treatment effects in SCLC. Together, our data demonstrate a fundamental role of Angiopoietin-2/Integrin beta-1 signaling in SCLC cells for tumor cell invasion and liver metastasis and provide a new effective treatment strategy for patients with SCLC.

2024-03-28 | GSE262409 | GEO

Claviceps fusiformis PRL 1980

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A macrophage autonomous alpha4beta1integrin-Syk-Rac2 signaling axis controls macrophage differentiation, tumor growth and metastasis

Project description:Macrophages, play an essential role in promoting tumor growth by affecting angiogenesis, immune suppression, invasion and metastasis. The signal transduction events within macrophages which encode the complex cascade of events required for tumor growth and polarization of macrophages are poorly understood. We have discovered an ECM dependent signaling pathway in macrophages that regulates M2 macrophage differentiation, tumor growth, invasion and metastasis. We provide direct evidence that a macrophage autonomous, M-NM-14M-NM-21 integrin dependent Syk-Rac2 signaling axis acts in concert with the p110 isoform (PTEN-PI-3 kinase pathway) to control metastasis. Bone marrow derived macrophages from five wild type and five Rac2 -/- mutant C57BL mice.

2012-10-02 | E-GEOD-41236 | biostudies-arrayexpress

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