The let-7 family of microRNAs.

By Sarah F. Roush, Frank J. Slack. Trends in Cell Biology, 2008

1,381 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/eea845846605f69c5f0605d2dea60162830ad382

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

In Molecular Biology

Citations in the corpus

Non‐coding RNAs: regulators of disease (2010, background): “The let-7 family of miRNAs is highly conserved throughout the Metazoa and functions as a master temporal regulator of development and differentiation, both in early embryos and complex adult tissues such as brain, in nematode, fruitfly, zebrafish and mouse [61–67].”
The widespread regulation of microRNA biogenesis, function and decay (2010, background): “Let-7 functions as a tumour suppressor by targeting several oncogenes, including MYC , KRAS and cyclin D1 ( CCND1”
Cardiac fibrosis in myocardial infarction—from repair and remodeling to regeneration (2016, background): “The Let-7 family of miRNAs also function as suppressors of stem cell pluripotency by regulating the expression of pluripotency genes Oct4 and Sox2 (Roush and Slack 2008).”
MicroRNAs: New Biomarkers for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Breast Cancer (2015, background): “let-7 miRNAs have been demonstrated to regulate multiple oncogenes, such as RAS, high-mobility group AT-hook 2 (HMGA2), c-Myc, and caspase-3 [177-180], and several genes involved in the maintenance of stem cell phenotype [181].”
Posttranscriptional regulation of microRNA biogenesis in animals. (2010, background): “While most let-7 pri-miRNA transcripts are highly expressed throughout development, the mature let-7 is detectable only in highly differentiated cells, suggesting a posttranscriptional regulation of biogenesis (Roush and Slack, 2008).”
miRNAs in human cancer (2010, background): “let-7 family Ubiquitous Multiple members (chromosomes 3, 9, 11, 19, 21, 22) TS CLL [119], lymphoma [120], gastric [121], lung [122], prostate [9], breast [123], ovarian [121], colon [121], leiomyoma [121], melanoma [121] miR-15a/16-1 cluster Ubiquitous 13q14.”
The Genetic Signatures of Noncoding RNAs (2009, background): “elegans, not in other organisms, despite the former being not only highly conserved in sequence and expression pattern throughout metazoan evolution [139], but also fundamental to normal and abnormal developmental processes [140– 142], as are many other miRNAs [143].”
Child health, developmental plasticity, and epigenetic programming. (2011, background): “Some of the first miRNAs that were discovered, such as the let-7 family of miRNAs, are master regulators of developmental differentiation, both in early embryos and adult tissues (103, 104).”
Improved classification of breast cancer by analysis of genetic alterations and gene expression profiling (2011, background): “up-regulation of mir-21 (reviewed in (11)), mir-17-92 cluster (reviewed in (12)), mir-26a (13), and down-regulation of let-7 family members (reviewed in (14)).”
Mesenchymal stem cell secretes microparticles enriched in pre-microRNAs (2009, background): “A most notable observation was that 9 of the 13 members in one of the most highly conserved and developmentally important human let-7 family (24,25) were expressed in MSCs.”
TUT4 in concert with Lin28 suppresses microRNA biogenesis through pre-microRNA uridylation. (2009, background): “let-7 has been implicated in cell differentiation in mammals (Bussing et al., 2008) and nematodes (Roush and Slack, 2008).”
MicroRNAs in human cancer. (2013, positive): “let-7/98 cluster Ubiquitous Multiple members (chromosomes 3, 9, 11, 19, 21, 22, X) TS CLL [ 136 ] , lymphoma [ 137 ] , gastric [ 138 ] , lung [ 139 ] , prostate [ 9 ] , breast [ 140 ] , ovarian [ 138 ] , colon [ 138 ] , leiomyoma [ 138 ] , melanoma [ 138 ]”
The Imprinted H19 LncRNA Antagonizes Let-7 MicroRNAs (2013, background): “Since high let-7 levels are generally associated with increased differentiated states (Roush and Slack, 2008), we hypothesized that H19 might serve to inhibit let-7 activity, thereby preventing precocious differentiation.”