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RECK Controls Breast Cancer Metastasis by Modulating a Convergent, STAT3-dependent Neoangiogenic Switch

ABSTRACT: Metastasis leads to the majority of deaths in breast cancer patients. Here we investigated the molecular and biochemical signaling pathways altered by RECK, a major metastasis suppressor gene in breast cancer. We overexpressed RECK in 2 highly invasive cell lines and knocked-down RECK expression in 2 poorly invasive cell lines. IPA analysis of differentially expressed genes revealed IL-6, and IL8 signaling alteration with RECK pertubation. This lead us to discover that RECK suppresses metastasis and neoangiogenesis at secondary sites by inhibiting STAT3 dependent VEGF & uPA regulating. This finding is significant because it reveals the biology behind a major metastasis suppressor gene in cancer. Cell lines were obtained from the ATCC or were generous gifts from Dr Joan Massague (MSKCC). Invasive cell lines were stably infected with a constitutively expressing RECK construct or and Empty Vector control. Poorly invasive cell lines were transfected with a Scramble siRNA or siRNA targeting the RECK gene. RNA was extracted using the RNeasy kit (Qiagen) as per the manufacturer’s instructions. Expression analysis was performed using the Affymetrics U133 2.0 microarray (Affymetrix). Affymetrix CEL files were imported into the Partek Genomics Suite (Partek).

ORGANISM(S): Homo sapiens

SUBMITTER: Logan Walsh

PROVIDER: E-GEOD-56898 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RECK Controls Breast Cancer Metastasis by Modulating a Convergent, STAT3-dependent Neoangiogenic Switch

Project description:Metastasis leads to the majority of deaths in breast cancer patients. Here we investigated the molecular and biochemical signaling pathways altered by RECK, a major metastasis suppressor gene in breast cancer. We overexpressed RECK in 2 highly invasive cell lines and knocked-down RECK expression in 2 poorly invasive cell lines. IPA analysis of differentially expressed genes revealed IL-6, and IL8 signaling alteration with RECK pertubation. This lead us to discover that RECK suppresses metastasis and neoangiogenesis at secondary sites by inhibiting STAT3 dependent VEGF & uPA regulating. This finding is significant because it reveals the biology behind a major metastasis suppressor gene in cancer.

2014-09-01 | GSE56898 | GEO

Molecular data integration reveals Growth Hormone Receptor as an alternative candidate oncogenic signaling pathway in glioblastoma

Project description:Our laboratory has identified the Growth Hormone Receptor (GHR) as a candidate oncogenic pathway involved in GBM oncogenicity. In order to study further the role of GHR in GBM, we have generated GHR overexpressing patient-derived cell lines (PDCL) from PDCL established by GlioTEx team (Institut du Cerveau et de la Moelle, Paris, France). An analysis of the global proteome of each variant was then undertaken. The wild-type (GHR WT) and constitutively activated (GHR CA) GHR expression vectors were generous gifts from Mike Waters and Peter Brooks (University of Queensland, Australia). The constitutively activated GHR vector was generated by fusing the transmembrane and cytoplasmic domains of rabbit GHR (to ensure the absence of human GH stimulation) to Jun zippers in order to achieve GH-independent forced dimerization in absence of the extracellular domain. The control GFP vector was obtained from Addgene . These vectors were then inserted in lentiviral vectors. Cells were transduced with multiplicity of infection of 20 and transduced cells were selected with puromycin.

2022-06-23 | PXD004969 | Pride

Expression data from ELK3 knocked down MDA-MB-231 cell line.

Project description:Triple-negative breast cancer is a highly aggressive tumor subtype that lacks effective therapeutic targets. Here, we show that ELK3 is overexpressed in a subset of breast cancers, in particular basal-like and normal-like/claudin-low cell lines. Suppression of ELK3 in MDA-MB-231 cells led to transdifferentiation from an invasive mesenchymal phenotype to a non-invasive epithelial phenotype both in vitro and in vivo. Suppression of ELK3 results in the extensive changes in genome expression profiles. Among these, GATA3, a master suppressor of metastasis, was epigenetically activated and we found that suppression of GATA3 led to the restoration of migration and invasion. These results suggest that the ELK3-GATA3 axis is a major pathway that promotes metastasis of MDA-MB-231 cells. Retrovirus expressing shRNA of ELK3 was transduced into MDA-MB-231 cell line and stable cell line of which ELK3 is suppressed more than 50% was selected by the drug selection (Puromycin).

2016-06-15 | E-GEOD-83325 | biostudies-arrayexpress

Expression data from ELK3 knocked down MDA-MB-231 cell line.

2016-06-15 | GSE83325 | GEO

Expression data from Mvt-1 clonal isolates over-expressing Ndn 50T or Ndn 50C

Project description:Ndn is a candidate metastasis suppressor gene that has been reported to regulate transcription. We examined the changes in gene expression caused by the stable over-expression of allelic variants of Ndn, 50T or 50C, using lentiviral transduction in the mouse mammary tumor cell line Mvt-1. A total of 9 samples were analyzed. In pairwise comparisons using Partek, genes with a Benjamini-Hochberg corrected p-value <0.05 and a fold-change â¥abs(2.5) were selected.

2016-02-08 | E-GEOD-65824 | biostudies-arrayexpress

Elevated MTSS1 mRNA Expression Is Associated with Metastasis and Poor Prognosis of Residual Hepatitis B-related Hepatocellular Carcinoma

Project description:Hepatectomy generally offers the best chance of long-term survival for patients with hepatocellular carcinoma (HCC). Many studies have shown that hepatectomy accelerates tumor metastasis, but the mechanism remains unclear. In this study, palliative hepatectomy was performed in an orthotopic nude mice model of HCC (MHCC97H) with high metastatic potential. Using Human Tumor Metastasis Microarray, we screened the metastasis-related genes in tumor tissues following palliative resection, and found that Metastasis suppressor 1 (MTSS1) located in the central position of gene function net of residual HCC; MTSS1 was up-regulated in residual tumor after palliative resection. Further studies found that MTSS1 enhanced the metastasis of residual HCC. In hepatitis B-related HCC patients undergone palliative hepatectomy, those with higher MTSS1 mRNA expression accompanied by the activation of matrix metalloproteinase 2 (MMP2) in residual HCC, had earlier residual HCC detection after hepatectomy and poorer survival when compared to those with lower MTSS1 level. In different cell lines, the levels of MTSS1 mRNA increased in parallel with metastatic potential. MTSS1 down regulation via siRNA decreased MMP2 activity, reduced invasive potentials of HCC by 28.9% in vitro, and averted the deteriorated lung metastatic extent in vivo. In conclusion, the poor prognosis of hepatitis B-related HCC patients following palliative hepatectomy associates with elevated MTSS1 mRNA expression; therefore, MTSS1 may provide a new research field for HCC diagnosis and treatment.

2015-12-15 | GSE75965 | GEO

Human Breast Cancer Cell Lines: Control vs. Fn14 or Luciferase siRNA Treated

Project description:We performed gene expression profiling on the MDA-MB-231 and MDA-MB-436 human breast cancer cell lines following siRNA-mediated inhibition of Fn14 expression as an approach to identify the mechanistic basis for Fn14 regulation of invasive capacity. Keywords: siRNA-mediated inhibition

2008-02-01 | GSE8871 | GEO

siRNA profiling of human cancer cell line MDA-MB-231 knocked down for CD146 mRNA

Project description:Metastasis is a complex process involving loss of adhesion, migration, invasion and proliferation of cancer cells. Cell adhesion molecules play a pivotal role in this phenomenon by regulating cell-cell and cell-matrix interactions. CD146 (MCAM) is associated with advanced tumor stage in melanoma, prostate and ovarian cancers. For this study, the MDA-MB-231 cell line was used as a prototypic mesenchymal and invasive cell line, spontaneously expressing high levels of CD146. Using whole-genome DNA microarrays, we investigated genes for which expression was modified by CD146 down-regulation, obtained by siRNA or shRNA technology Experiment Overall Design: Expression profiles of two cell lines transfected by two differents ShRNA directed against CD146 were compared with expression profiles of 3 control cell lines (i.e. native cell line, empty plasmid and shRNA directed against GFP)

2008-10-21 | E-GEOD-11951 | biostudies-arrayexpress

KDM4A regulated genes in human squamous carcinoma cells

Project description:To establish a robust cellular model system for screening genes associated with cell invasion, we over-expressed the oncogenic translocated promoter region (Tpr)-MET proteins in SCC23 cells (SCC23/MET). Using a functional siRNA screen, we identified that the histone demethylase KDM4A played a critical role in the invasive growth and metastasis of SCC mediated by the Oncogenic MET. To investigate the molecular mechanism through which KDM4A inhibit the tumor cell invasion, we knock-down KDM4A in SCC23/MET cell and performed a gene microarray to examine which genes may be regulaged by kDM4A. We generated two stable cell lines. one was infected with virus containing scramble and another infected with virus infected with virus containing KDM4A shRNA. Total RNA were extracted from these two cell lines and subject to microarray.

2013-05-03 | E-GEOD-44238 | biostudies-arrayexpress

Identification and Validation of Genes with Expression Patterns Inverse to Multiple Metastasis Suppressor Genes in Breast Cancer Cell Lines

Project description:Metastasis suppressor genes (MSGs) have contributed to an understanding of regulatory pathways unique to the lethal metastatic process. When re-expressed in experimental models, MSGs block cancer spread to, and colonization of distant sites without affecting primary tumor formation. On a single MSG basis, genes have been identified with expression patterns inverse to a MSG, and found to encode functional, druggable signaling pathways. We now hypothesize that common signaling pathways mediate the effects of many MSGs. By gene expression profiling of human MCF7 breast carcinoma cells expressing a scrambled siRNA or siRNAs to each of 19 validated MSGs (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1), we identified genes whose expression was significantly opposite to at least five MSGs. We used microarrays to evaluate the modification in gene expression profile after donregulation of multiple metastasis suppressors (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1) in the breast cancer cell line, MCF7. MCF7 cell line was transfected with siRNA targeting each of 19 metastasis suppressors (NME1, BRMS1, CD82, CDH1, CDH2, CDH11, CASP8, MAP2K4, MAP2K6, MAP2K7, MAPK14, GSN, ARHGDIB, AKAP12, DRG1, CD44, PEBP1, RRM1, KISS1). Two siRNA sequences (siRNA1 and siRNA2) were used for each metastasis suppressor. Two time points (48hr and 96hr) were considered as end of transfection in order to measure early and late effects of the metastasis suppressors downregulation.

2013-12-27 | E-GEOD-53668 | biostudies-arrayexpress

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