Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA121463 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs) have emerged as important gene regulators and are recognized as key players in tumorigenesis. miR-145 is reported to be down-regulated in several cancers, but knowledge of its targets in colon cancer remains limited. To investigate the role of miR-145 in colon cancer, we have employed a microarray based approach to identify miR-145 targets. Based on seed site enrichment analyses and unbiased word analyses, we found a significant enrichment of miRNA binding sites in the 3’-untranslated regions (UTRs) of transcripts down-regulated upon miRNA overexpression, which represent potential miR-145 targets. Gene Ontology analysis showed an overrepresentation of genes involved in cell death, gene expression, cancer, cell cycle, DNA replication, recombination and repair. A number of the identified miRNA targets have previously been implicated in cancer, including YES, FSCN1, ADAM17, BIRC2, VANGL1 as well as the transcription factor STAT1. Both YES and STAT1 were verified as direct miR-145 targets based on 3’UTR luciferase assays and western blots for endogenous proteins.
2010-10-01 | GSE18625 | GEO
Project description:MicroRNAs (miRNAs) have emerged as important gene regulators and are recognized as key players in tumorigenesis. miR-145 is reported to be down-regulated in several cancers, but knowledge of its targets in colon cancer remains limited. To investigate the role of miR-145 in colon cancer, we have employed a microarray based approach to identify miR-145 targets. Based on seed site enrichment analyses and unbiased word analyses, we found a significant enrichment of miRNA binding sites in the 3’-untranslated regions (UTRs) of transcripts down-regulated upon miRNA overexpression, which represent potential miR-145 targets. Gene Ontology analysis showed an overrepresentation of genes involved in cell death, gene expression, cancer, cell cycle, DNA replication, recombination and repair. A number of the identified miRNA targets have previously been implicated in cancer, including YES, FSCN1, ADAM17, BIRC2, VANGL1 as well as the transcription factor STAT1. Both YES and STAT1 were verified as direct miR-145 targets based on 3’UTR luciferase assays and western blots for endogenous proteins. DLD-1 cells were transfected with 50 nM miR-145 duplex or mock transfected. Total RNA was harvested 24 hours post-transfection and analyzed on Affymetrix HG-U133 Plus 2.0 human arrays.
2010-10-01 | E-GEOD-18625 | biostudies-arrayexpress
Project description:miR-145 is a tumor suppressor miRNA in various malignancies including pancreatic cancer. Identification of miR-145 targets can lead to more understanding of the development of pancreatic cancer. Therefore, in this project, we aimed to characterize the changes of transcriptomes caused by miR-145 to identify more miR-145 target transcripts.
2013-03-19 | GSE45245 | GEO
Project description:miR-145 is a tumor suppressor miRNA in various malignancies including pancreatic cancer. Identification of miR-145 targets can lead to more understanding of the development of pancreatic cancer. Therefore, in this project, we aimed to characterize the changes of transcriptomes caused by miR-145 to identify more miR-145 target transcripts. cDNA microarray was used to compare transcriptomes 48 hr after transfection of miR-145 mimics or control scramble RNA in a pancreatic cancer cell line, Mia-PaCa2.
2013-03-19 | E-GEOD-45245 | biostudies-arrayexpress
Project description:Identification of miR-145 or miR-133a target genes in bladder cancer
| PRJNA121911 | ENA
Project description:miR-145 is downregulated in multiple cancers. The introduction of miR-145 could alleviate the tumor burden in the pancreatic cancer mouse model. However, how miR-145 mediates the tumor suppression is still an open question. In this study, we aimed to identify the targets of miR-145 using a SILAC approach.
2014-10-28 | PXD001260 | Pride
Project description:Identification of Sp1 targets involved in proliferation and cancer
| PRJNA165827 | ENA
Project description:An increasing number of studies have shown that long noncoding RNA (lncRNA) dysregulation plays an important role in development of various cancers, including colon cancer. Nonetheless, the potential mechanisms of lncRNA in regorafenib-resistance remain unclear. Our research revealed the lncRNA AC069513.3 (MIR570MG) increased in regorafenib-resistant colon cancer cells compared to the regorafenib-sensitive cells. Furthermore, lncRNA AC069513.3 (MIR570MG) sponged miR-145, which declined in regorafenib-resistant colon cancer cell lines. More importantly, overexpression of miR-145 hampered cell proliferation and retrieved colon cancer regorafenib-sensitivity, contrary to the function of lncRNA AC069513.3 (MIR570MG). Dual luciferase reporter assay confirmed that miR-145 bound to 3’-UTR of SMAD3, a transcriptional modulator activated by TGFβ, resulting in blockage of TGFβ /SMAD3-mediated cell growth and cycle progression. Furthermore, ectopic expression of miR-145 inhibitor in the parental cells endowed resistance to regorafenib. Conversely, knockdown of AC069513.3 (MIR570MG) impoverished resistance against regorafenib. In summary, our findings suggested that lncRNA AC069513.3 (MIR570MG) promoted regorafenib resistance via releasing SMAD3 from miR-145, leading to activation of SMAD3-mediated signaling pathways. Long noncoding RNA profiling by RT-PCR
2020-02-11 | GSE141134 | GEO
Project description:miRNAs regulation by miR-145 in pancreatic cancer
| PRJNA193313 | ENA