DOI . ORG {
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We began analyzing https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0039102, but it redirected us to https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0039102. The analysis below is for the second page.
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Description:
ERRα is an orphan nuclear receptor emerging as a novel biomarker of breast cancer. Over-expression of ERRα in breast tumor is considered as a prognostic factor of poor clinical outcome. The mechanisms underlying the dysexpression of this nuclear receptor, however, are poorly understood. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level and play important roles in tumor initiation and progression. In the present study, we have identified that the expression of ERRα is regulated by miR-137, a potential tumor suppressor microRNA. The bioinformatics search revealed two putative and highly conserved target-sites for miR-137 located within the ERRα 3′UTR at nt 480–486 and nt 596–602 respectively. Luciferase-reporter assay demonstrated that the two predicted target sites were authentically functional. They mediated the repression of reporter gene expression induced by miR-137 in an additive manner. Moreover, ectopic expression of miR-137 down-regulated ERRα expression at both protein level and mRNA level, and the miR-137 induced ERRα-knockdown contributed to the impaired proliferative and migratory capacity of breast cancer cells. Furthermore, transfection with miR-137mimics suppressed at least two downstream target genes of ERRα–CCNE1 and WNT11, which are important effectors of ERRα implicated in tumor proliferation and migration. Taken together, our results establish a role of miR-137 in negatively regulating ERRα expression and breast cancer cell proliferation and migration. They suggest that manipulating the expression level of ERRα by microRNAs has the potential to influence breast cancer progression.
Title[redir]:
No title found...
Description:
ERRα is an orphan nuclear receptor emerging as a novel biomarker of breast cancer. Over-expression of ERRα in breast tumor is considered as a prognostic factor of poor clinical outcome. The mechanisms underlying the dysexpression of this nuclear receptor, however, are poorly understood. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level and play important roles in tumor initiation and progression. In the present study, we have identified that the expression of ERRα is regulated by miR-137, a potential tumor suppressor microRNA. The bioinformatics search revealed two putative and highly conserved target-sites for miR-137 located within the ERRα 3′UTR at nt 480–486 and nt 596–602 respectively. Luciferase-reporter assay demonstrated that the two predicted target sites were authentically functional. They mediated the repression of reporter gene expression induced by miR-137 in an additive manner. Moreover, ectopic expression of miR-137 down-regulated ERRα expression at both protein level and mRNA level, and the miR-137 induced ERRα-knockdown contributed to the impaired proliferative and migratory capacity of breast cancer cells. Furthermore, transfection with miR-137mimics suppressed at least two downstream target genes of ERRα–CCNE1 and WNT11, which are important effectors of ERRα implicated in tumor proliferation and migration. Taken together, our results establish a role of miR-137 in negatively regulating ERRα expression and breast cancer cell proliferation and migration. They suggest that manipulating the expression level of ERRα by microRNAs has the potential to influence breast cancer progression.
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Keywords {🔍}
errα, cancer, cell, breast, expression, cells, article, view, target, google, scholar, level, receptor, skbr, utr, transfection, gene, mrna, analysis, tumor, ccne, protein, proliferation, reporter, cycle, data, mdamb, estrogenrelated, mimics, fig, luciferase, human, lines, assay, rna, activity, performed, alpha, microrna, genes, plos, control, figure, image, wnt, line, effect, treatment, progression, signaling,
Topics {✒️}
health open-access article distributed estrogen-related receptor-gamma estrogen-related receptor alpha cookies plos plos contributed reagents/materials/analysis tools estrogen receptor alpha errα/β-cat complex multiple-hormone response element dual-luciferase reporter system estrogen-related receptor 3 cell-specific biological function sk-br-3 cell line erα-positive/her2-negative erα-negative/her2-positive mda-mb-231 cell line orphan nuclear receptor poor-prognosis breast carcinoma quantitative-real-time pcr estrogen receptor-positive highly conserved target-sites erα-positive/her2-positive tumorigenesis-related target genes her2-positive breast cancer endocrine-responsive breast cancer original author 100ng/ml cholera toxin estrogen-related receptors reverse transcriptase m-mlv positive auto-regulatory loop rnu6b-small nuclear rna site-directed mutagenesis kit normal breast epithelial erbb2/her2 signaling pathway ligand-independent transcriptional activation sk-br-3 cells partly estrogen signaling pathway luciferase-reporter assay demonstrated methods rna oligonucleotides human breast carcinoma sk-br-3 cells transfected mda-mb-231 cells partly brdu incorporation assay cancer cell proliferation tumor-suppressive micrornas silenced cell proliferation assay β-actin mrna expression firefly luciferase gene squamous cell carcinoma
Questions {❓}
- (2006) Which cyclin E prevails as prognostic marker for breast cancer?
- However, besides at transcriptional level, are there any regulatory mechanisms at additional levels?
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