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Involvement of transcription factor early growth response 4 (EGR4) in lung cancer bone metastasis

ABSTRACT: EGR4 (early growth response 4), a transcription factor, was previously shown to be up-regulated in lung cancer bone metastasis, compared with its expression in metastasis in other organs, using a multiorgan metastasis model of human small-cell lung cancer cells (SBC-5) in NK cell-depleted SCID mice (Kakiuchi S et al. Mol Cancer Res 2003). Here we show that EGR4 was essential for survival cancer cells, and migration ability. Next, in searching of downstream genes regulated by EGR4, we analyzed the changes in transcriptomes of SBC-5 cells at different time-points (24, 48 and 72 hr) when knockdown of EGR4 by siRNA. Lots of genes were identified either up-regulated or down-regulated in siEGR4 samples compared with control siRNA. Among these genes, there were genes with roles in metastasis or bone biology. The fact that EGR4 knockdown led to up-regulation or suppression of these genes also indicated dual roles of EGR4 in transcriptional regulation, which is consistent with previous reports: EGR4 may repress its own promoter (Zipfel PF et al. Biochim Biophys Acta. 1997) or activate certain inflammatory genes (Decker EL et al. Nucleic Acids Res. 2003; Wieland GD et al. J Cell Sci. 2005).

ORGANISM(S): Homo sapiens

PROVIDER: GSE40558 | GEO | 2013/04/01

SECONDARY ACCESSION(S): PRJNA174294

REPOSITORIES: GEO

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Involvement of transcription factor early growth response 4 (EGR4) in lung cancer bone metastasis

Project description:EGR4 (early growth response 4), a transcription factor, was previously shown to be up-regulated in lung cancer bone metastasis, compared with its expression in metastasis in other organs, using a multiorgan metastasis model of human small-cell lung cancer cells (SBC-5) in NK cell-depleted SCID mice (Kakiuchi S et al. Mol Cancer Res 2003). Here we show that EGR4 was essential for survival cancer cells, and migration ability. Next, in searching of downstream genes regulated by EGR4, we analyzed the changes in transcriptomes of SBC-5 cells at different time-points (24, 48 and 72 hr) when knockdown of EGR4 by siRNA. Lots of genes were identified either up-regulated or down-regulated in siEGR4 samples compared with control siRNA. Among these genes, there were genes with roles in metastasis or bone biology. The fact that EGR4 knockdown led to up-regulation or suppression of these genes also indicated dual roles of EGR4 in transcriptional regulation, which is consistent with previous reports: EGR4 may repress its own promoter (Zipfel PF et al. Biochim Biophys Acta. 1997) or activate certain inflammatory genes (Decker EL et al. Nucleic Acids Res. 2003; Wieland GD et al. J Cell Sci. 2005). SBC-5 cells were cultured at 1x10^6 cells/2 ml in 3.5 cm plate. After seeding 24 hours, cells were transfected either siEGR4 or siEGFP (for control), using Lipofectamin. At 24, 48 and 72 hours after starting of siRNA, we extracted RNA from these cells, and subjected these RNAs to microarray analysis. The labeling, amplification, hybridization and microarray data analysis were described previously (Dat LT et al. Int J Oncol, 40: 1455-1469 2012).

2013-04-01 | E-GEOD-40558 | biostudies-arrayexpress

acute genes during CNS injury and their expression in cultured astrocytes

Project description:A robust set of CNS transcript changes was defined by comparing microarray data that describe the injury response of the rat retina [Vazquez-Chona et al., IOVS 2004; GSE1001], brain [Matzilevich et al., J Neurosci Res 2002; GSE1911], and spinal cord [Di Giovanni et al., Ann Neurol 2003; GDS63]. We determined the CNS injury genes that were expressed in cultured astrocytes from rat cortex [GSM34300] and from human optic nerve head [Yang et al., Physiol Genomics 2004; GDS532]. Keywords: other

2005-07-01 | GSE1928 | GEO

Microarray screening of RNA samples from low-, intermediate- and high-passage human prostate LNCaP cells

Project description:This laboratory studies the structures, biosynthesis, and functions of mucin glycans The low-(<33) and high-(>80)passage human prostate LNCaP cells developed by Dr. Ming-Fong Lin (Lin et al, Urology 166:1943, 2001) have been considered as the best in vitro model that reflects the progression of prostate cancer from androgen-dependent to androgen-independent stage (Parajuli et al, Cancer Res. 61:8227, 2001; Demeade et al, The Prostate 54:249, 2003; Unni et al, Cancer Res. 64:7156, 2004). The high-passage cells are metastatic while the low-passage cells are not. RT-PCR analysis of these two cell clones for 25 glycogenes among 8 different groups of glycogenes showed that only high-passage cells expressed two (isozymes 1 and 5) of the five known GlcNAc6ST genes. In addition, P-selectin blot analysis showed qualitative and quantitative differences between these clones. They included 3 higher intensity bands and 3 lower intensity bands in high-passage cells as compared to low-passage cells. The difference in P-selectin-specific glycoconjugates between low and high-passage LNCaP cells should help identify the glycans that distinguish high- from low-passage LNCaP cells.

2011-04-29 | GSE28927 | GEO

Discovery of genes regulated by the metastasis suppressor gene, RhoGDI2

Project description:A number of studies find that metastasis suppressor proteins, including RhoGDI2, may function in part though controlling expression of genes regulating metastasis (reviewed in Smith and Theodorescu, Nature Reviews Cancer, 2009, PMID: 19242414). To uncover systematically gene expression patterns dependent on RhoGDI2 expression, we profiled gene expression in stably transfected control (GFP empty vector) UM-UC-3 bladder carcinoma cells (which have lost endogenous expression of RhoGDI2, as occurs commonly in the progression of bladder cancer PMID: 15173088), as well as stably transfected GFP-tagged RhoGDI2 expressing UM-UC-3 cells. References: Moissoglu K, McRoberts KS, Meier JA, Theodorescu D et al. Rho GDP dissociation inhibitor 2 suppresses metastasis via unconventional regulation of RhoGTPases. Cancer Res 2009 Apr 1;69(7):2838-44. PMID: 19276387 Wu Y, Moissoglu K, Wang H, Wang X et al. Src phosphorylation of RhoGDI2 regulates its metastasis suppressor function. Proc Natl Acad Sci U S A 2009 Apr 7;106(14):5807-12. PMID: 19321744 Smith SC, Theodorescu D. Learning therapeutic lessons from metastasis suppressor proteins. Nat Rev Cancer 2009 Apr;9(4):253-64. PMID: 19242414 Theodorescu D, Sapinoso LM, Conaway MR, Oxford G et al. Reduced expression of metastasis suppressor RhoGDI2 is associated with decreased survival for patients with bladder cancer. Clin Cancer Res 2004 Jun 1;10(11):3800-6. PMID: 15173088

2012-04-15 | GSE35014 | GEO

Expression analysis of C. elegans genes kin-1 and crh-1 mutant

Project description:Investigation of whole genome gene expression level changes in C. elegans genes kin-1 and crh-1 mutant, compared to the wild-type strain. NimbleScan software’s implementation of RMA offers quantile normalization and background correction. There are three steps of RMA: Firstly, background subtraction was performed using a local background estimator. Secondly, quantile normalization (Bioinformatics 2003; 19:185) at probe level was done to make the expression distributions the same for all arrays. Last, probe set summarization was performed using Robust Multichip Average (RMA) algorithm as described by Irizarry, et al. (Nucleic Acids Res. 2003; 31:e15 and Biostatistics 2003; 4:249).

2012-09-13 | GSE40809 | GEO

Expression analysis of C. elegans genes daf-9 and daf-12 mutant

Project description:Investigation of whole genome gene expression level changes in C. elegans genes daf-9 and daf-12 mutant,compared to the wild-type strain NimbleScan software’s implementation of RMA offers quantile normalization and background correction. There are three steps of RMA: Firstly, background subtraction was performed using a local background estimator. Secondly, quantile normalization (Bioinformatics 2003; 19:185) at probe level was done to make the expression distributions the same for all arrays. Last, probe set summarization was performed using Robust Multichip Average (RMA) algorithm as described by Irizarry, et al. (Nucleic Acids Res. 2003; 31:e15 and Biostatistics 2003; 4:249).

2012-10-18 | GSE41661 | GEO

Discovery of genes regulated by the metastasis suppressor gene, RhoGDI2

2012-04-14 | E-GEOD-35014 | biostudies-arrayexpress

MicroRNA expression in prostate cancer cells stimulated with cancer associated fibroblasts

Project description:Tumor microenvironment is a strong determinant for the acquisition of metastatic potential of cancer cells. It has been demonstrated (Giannoni E et al., Cancer Res 2010) that cancer associated fibroblasts (CAF) elicit an epithelial-mesenchymal transition (EMT) in prostate cancer (PCa) cells, leading to enhanced tumor cell aggressiveness. Here, we investigated the involvement of microRNAs (miRNA) in such malignant tumor-stroma interplay, to identify possible tools to counteract metastasis dissemination.

2013-09-01 | GSE42699 | GEO

Transcription profiling of rat astrocytes in culture and from human optic nerve to identify acutely expressed genes during CNS injury and their expression in cultured astrocytes

2008-06-11 | E-GEOD-1928 | biostudies-arrayexpress

Nuclear Factor I/B is an Oncogene in Small Cell Lung Cancer

Project description:Small cell lung cancer (SCLC) is an aggressive cancer often diagnosed only after it has metastasized to distant sites (Meuwissen and Berns 2005; Cooper and Spiro 2006). Despite the need to better understand this disease, SCLC remains poorly characterized at the molecular and genomic levels (Forgacs et al. 2001; Pleasance et al. 2010). Using a genetically-engineered mouse model of SCLC driven by conditional deletion of Trp53 and Rb1 in the lung (Jonkers et al. 2001; Vooijs et al. 2002; Meuwissen et al. 2003; Sage et al. 2003), we identified several frequent, high-magnitude focal DNA copy number alterations in SCLC. We uncovered amplification of a novel, oncogenic transcription factor, Nuclear Factor I/B (Nfib) in the mouse SCLC model and in human SCLC. Functional studies indicate that NFIB regulates cell viability and proliferation during transformation.

2011-12-08 | GSE29533 | GEO

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