Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA145819 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ECRG4 is a promising tumor suppressor gene (TSG) recently identified in esophageal carcinoma. Its expression and prognostic value have never been explored in breast cancer. Using DNA microarray, we examined ECRG4 mRNA expression in 353 invasive breast cancer samples. A meta-analysis was performed on a large public retrospective gene expression dataset (n=1,387) to analyze correlation between ECRG4 expression and histo-clinical features including survival.
2011-12-02 | GSE31448 | GEO
Project description:Esophageal cancer-related gene 4 (Ecrg4), a hormone-like peptide, is thought to be a tumor suppressor, however little is known about the mechanism of how Ecrg4 suppresses tumorigenesis. Using the mouse glioma–initiating cell models, we identified Ecrg4 acts as a tumor suppressor in vivo. To characterize the function of Ecrg4 towards microglia, an innate immune cell in central nervous system, we performed gene expression microarray analysis for primary microglia treated with or without recombinant Fc-fused Ecrg4 fragments. We demonstrate here that Ecrg4 fragments, amino acid residues 71-132 and 133-148, which are produced by the proteolitic cleavage, induced the expression of pro-inflammatory cytokines in microglia. Thus, Ecrg4 acts as a cytokine/chemokine inducer, which activates the immune cells to eradicate tumor.
2016-09-28 | GSE87376 | GEO
Project description:Esophageal cancer-related gene 4 (Ecrg4) encodes a hormone-like peptide, and is thought to be involved in a variety of physiological phenomena including tumor suppressor function. Recent progress of Ecrg4 reveals that Ecrg4 peptides are pro-inflammatory and induce the expression of several cytokines and chemokines. However, detailed molecular mechanisms of Ecrg4 signaling, especially the receptors for Ecrg4 peptides, remain poorly understood. Here, using retrovirus-mediated expression cloning, we identified lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as a membrane protein bound for amino acid residues 71-132 of Ecrg4, Ecrg4(71-132). Moreover, not only LOX-1 but also several scavenger receptors such as Scarf1, Cd36 and Stabilin-1 efficiently internalized Ecrg4(71-132) into cells. The broad scavenger receptor competitive inhibitor polyinosinic acid reduced both the internalization of Ecrg4(71-132) and activation of NF-kB in microglia. In addition, this activation is dependent on Myd88, an adaptor protein to recruit signaling proteins to TLR and IL-1R receptors with induction of several immune response. These data suggest that multiple scavenger receptors recognize Ecrg4(71-132) and transduce its signals along with TLR/IL-1R receptors in microglia.
2018-03-23 | GSE106400 | GEO
Project description:The transcription factor c-Myb has been well characterized as an oncogene in several human tumor types, and its expression in the hematopoietic stem/progenitor cell population is essential for proper hematopoiesis. However, the role of c-Myb in mammopoeisis and breast tumorigenesis is poorly understood, despite its high expression in the majority of breast cancer cases (60-80%). We find that c-Myb high expression in human breast tumors correlates with the luminal/ER+ phenotype and a good prognosis. RNAi knock-down of endogenous c-Myb levels in the MCF7 luminal breast tumor cell line increases tumorigenesis both in vitro and in vivo, suggesting a tumor suppressor role in luminal breast cancer. We created a mammary-derived c-Myb expression signature and found it to be highly correlated with a published mature luminal mammary cell signature and least correlated with a mammary stem/progenitor lineage gene signature. These data describe, for the first time, a tumor suppressor role for the c-Myb proto-oncogene in breast cancer that has implications for understanding luminal tumorigenesis and for guiding treatment. refXsample
2010-10-15 | E-GEOD-21371 | biostudies-arrayexpress
Project description:In this study, we identify leucyl-tRNA synthetase (LARS) as a breast tumor suppressor. To identify the mechanism underlying LARS-mediated breast tumor suppression, we conducted TMT-proteomics in PyMT mouse tumors with monoallelic genetic deletion of LARS in the mammary tumor compartment. The analyses implicate LARS as a regulator of leucine-rich protein translation resulting in downregulation of candidate leucine-rich tumor suppressor genes.
2022-01-10 | PXD026609 | Pride
Project description:To investigate the role of FLRT2 in breast cancer, its expression was knocked down and upregulated in mammary cell lines. Our results show that FLRT2 has tumor suppressor activity in breast cancer.
2016-12-30 | GSE85247 | GEO
Project description:MicroRNAs (miRs) are small non-coding RNAs that can function as tumor suppressor genes. We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent dataset and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the candidate tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer cells. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair, and actin dynamics. This observation was further corroborated with protein expression analysis and 3’-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters gH2A.X marker expression and affects the cellular organization of F-actin and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility. In this study we monitored global miRNA expression changes in prostate cancer LNCaP cells treated with the epigenetic compounds 5-Azacytidine (5-AzaC) and/or trichostatin A (TSA). Cells were treated with epigenetic drugs for 36 hours and total RNA was isolated for hybridization to miRNA microarrays. 5 independent experiments were performed (n=4 for combined treatment). The candidate prostate tumor suppressor miRNAs, miR-1, miR-206, and miR-27 were up-regulated in LNCaP cells for Affymetrix microarray analysis. LNCaP cells were transfected with pre-miR oligos and 24 hr post-transfection total RNA was collected for microarray analysis; total of three independent experiments.
2011-12-01 | E-GEOD-31620 | biostudies-arrayexpress
Project description:Chromosomal structural mutations play an important role in determining the transcriptional landscape of human breast cancers. To assess the nature of these structural mutations, we analyzed a representative sampling of the major types of breast tumor samples for detailed structural mutations using paired-end tag sequencing of long-insert genomic DNA (DNA-PET) with matched transcriptome ascertainment by RNA-seq. Compared with other structural mutations, tandem duplications are enriched around partners of fusion transcripts and demarcate regions of high gene expression. Moreover tandem duplications appear to be early events in tumor evolution by facilitating subsequent downstream amplification and deletion of important adjacent cancer associated genes. In a detailed reconstruction of events in chr17, we found large unpaired-inversions connect a duplicated ERBB2 with neighboring 17q21.3 amplicons while simultaneously deleting the intervening BRCA1 tumor suppressor locus. Using siRNAs in breast cancer cell lines, we showed that the 17q21.3 amplicon harbored a significant number of weak oncogenes that appeared consistently co-amplified in primary tumors. Down-regulation of BRCA1 expression augmented the cell proliferation in human normal mammary epithelial cells. Finally, using in silico approaches, we determined that genes whose expression in breast tumors are associated with either poor or good clinical prognosis appear clustered together in segments of frequent amplification or deletion, suggesting that structural abnormalities induce the loss or gain of blocks of adjacent genes with oncogenic or growth suppressor function. These analyses suggest that structural mutations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously. RNA sequencing of four primary breast cancer RNA samples (SOLiD, Applied Biosystems).
2014-07-01 | E-GEOD-57914 | biostudies-arrayexpress
Project description:The SLC22A18 gene, which encodes an orphan transporter, is located at the 11p15.5 imprinted region, an important tumor-suppressor gene region. However, the role of SLC22A18 in tumor suppression remains unclear. Here, we investigated the involvement of SLC22A18 in cell growth, invasion and drug resistance of MCF7 human breast cancer cell line. Western blot analysis indicated that SLC22A18 is predominantly expressed at intracellular organelle membranes. Quantitative proteomics showed that knockdown of SLC22A18 significantly altered the expression of 578 (31.0%) out of 1867 proteins identified, including proteins related to malignancy and poor prognosis of breast cancer.
2019-06-01 | PXD010183 | JPOST Repository
Project description:Pre-operative progesterone intervention has been shown to confer a survival benefit to breast cancer patients independent of their progesterone receptor (PR) status, raising a question about how progesterone affects the outcome of PR-negative cells. Here, we identify up-regulation of a Serum- and glucocorticoid-regulated kinase gene, SGK1 and an N-Myc Downstream Regulated Gene 1, NDRG1, along with down-regulation of miR-29a and miR-101-1 targeting 3’UTR region of SGK1, to differential extents in a PR dependent manner in breast cancer cells. We further demonstrate a novel dual-phase transcriptional and post-transcriptional regulation of SGK1 in response to progesterone leading to up-regulation of a tumor metastasis suppressor gene, NDRG1, mediated by a set of AP-1 network genes. The NDRG1 further inactivates a set of kinases impeding the invasion and migration of breast cancer cells. In summary, we propose a model for the mode of action of progesterone in breast cancer deciphering the molecular basis of a randomized clinical trial studying the effect of progesterone in breast cancer with a potential to improve the prognosis of breast cancer patients for receiving pre-operative progesterone treatment.
2018-10-19 | E-MTAB-6742 | biostudies-arrayexpress