Cooperative interplay of let-7 mimic and HuR with <i>MYC</i> RNA

Gunzburg, Menachem J.; Sivakumaran, Andrew; Pendini, Nicole R.; Yoon, Je‐Hyun; Gorospe, Myriam; Wilce, Matthew C. J.; Wilce, Jacqueline Anne

doi:10.1080/15384101.2015.1069930

Cited by 19 publications

(16 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Moreover, HuR, RNA-binding protein, binds and represses MYC mRNA by recruiting the let-7 /RISC complex to 3′ UTR region of MYC (Ma et al, 1996 ; Kim et al, 2009 ). In addition, recruitment of HuR and let-7 to the transcript of MYC is interdependent (Kim et al, 2009 ; Gunzburg et al, 2015 ). Interestingly, MYC can also negatively regulate let-7 family members such as let-7a , - 7d , and - 7g by binding to their promoters, thus, forming a negative-feedback loop (Chang et al, 2008 ; Wang et al, 2011 ).…”

Section: General Features Of the Let-7 Familymentioning

confidence: 99%

Biogenesis and regulation of the let-7 miRNAs and their functional implications

et al. 2015

View full text Add to dashboard Cite

The let-7 miRNA was one of the first miRNAs discovered in the nematode, Caenorhabditis elegans, and its biological functions show a high level of evolutionary conservation from the nematode to the human. Unlike in C. elegans, higher animals have multiple isoforms of let-7 miRNAs; these isoforms share a consensus sequence called the ‘seed sequence’ and these isoforms are categorized into let-7 miRNA family. The expression of let-7 family is required for developmental timing and tumor suppressor function, but must be suppressed for the self-renewal of stem cells. Therefore, let-7 miRNA biogenesis must be carefully controlled. To generate a let-7 miRNA, a primary transcript is produced by RNA polymerase II and then subsequently processed by Drosha/DGCR8, TUTase, and Dicer. Because dysregulation of let-7 processing is deleterious, biogenesis of let-7 is tightly regulated by cellular factors, such as the RNA binding proteins, LIN28A/B and DIS3L2. In this review, we discuss the biological functions and biogenesis of let-7 miRNAs, focusing on the molecular mechanisms of regulation of let-7 biogenesis in vertebrates, such as the mouse and the human.

show abstract

Section: General Features Of the Let-7 Familymentioning

confidence: 99%

Biogenesis and regulation of the let-7 miRNAs and their functional implications

et al. 2015

View full text Add to dashboard Cite

show abstract

“…HuR has been shown to increase the stability of transcripts involved in carcinogenesis, cell proliferation and survival, and oxidative and genotoxic cellular response (Fan et al, ; Y. Li, Estep, & Karginov, ). Some of those transcripts include proto‐oncogenes c‐Fos (C. Y. Chen, Xu, & Shyu, ) and c‐Myc (Gunzburg et al, ); cyclooxygenase‐2 (COX‐2; Doller et al, ); iNOS (Z. Guo & Geller, ); tumor suppressors TP53 (Abdelmohsen et al, ) and von Hippel–Lindau (Galbán et al, ). Interestingly, HuR can also regulate APA of target genes dependent on U‐rich sequences proximal to poly(A) signal (Barnhart, Moon, Emch, Wilusz, & Wilusz, ; Berkovits & Mayr, ; Zhu, Zhou, Hasman, & Lou, ), of genes involved in stress responses (Kraynik et al, ), and of its own gene through reduction of CstF‐64 recruitment (Dai, Zhang, & Makeyev, ).…”

Section: Deadenylation: Rbps and Micrornasmentioning

confidence: 99%

Connections between 3′ end processing and DNA damage response: Ten years later

Murphy

Kleiman

2019

WIREs RNA

View full text Add to dashboard Cite

Ten years ago we reviewed how the cellular DNA damage response (DDR) is controlled by changes in the functional and structural properties of nuclear proteins, resulting in a timely coordinated control of gene expression that allows DNA repair. Expression of genes that play a role in DDR is regulated not only at transcriptional level during mRNA biosynthesis but also by changing steady‐state levels due to turnover of the transcripts. The 3′ end processing machinery, which is important in the regulation of mRNA stability, is involved in these gene‐specific responses to DNA damage. Here, we review the latest mechanistic connections described between 3′ end processing and DDR, with a special emphasis on alternative polyadenylation, microRNA and RNA binding proteins‐mediated deadenylation, and discuss the implications of deregulation of these steps in DDR and human disease. This article is categorized under: RNA Processing > 3′ End Processing RNA‐Based Catalysis > Miscellaneous RNA‐Catalyzed Reactions RNA in Disease and Development > RNA in Disease

show abstract

“…Additional studies are needed to define the underlying mechanism by which HuR inhibits the expression of certain miRNAs. One possible explanation is that HuR cooperates with the miRNA let-7 in down-regulating the expression of c-Myc (48,49), a transcription factor that promotes microRNA biogenesis (50), and thus knock-out of HuR may increase c-Myc expression, which, in turn, promotes expression of microRNAs. This possibility remains to be tested experimentally.…”

Section: Hur Regulates Ccr6 Expression On Th17 Cellsmentioning

confidence: 99%

The RNA-binding protein HuR contributes to neuroinflammation by promoting C-C chemokine receptor 6 (CCR6) expression on Th17 cells

Chen

Martindale

Cramer

et al. 2017

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

In both multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), the C-C chemokine receptor 6 (CCR6) is critical for pathogenic T helper 17 (Th17) cell migration to the central nervous system (CNS). Whereas many cytokines and their receptors are potently regulated via post-transcriptional mechanisms in response to various stimuli, how CCR6 expression is post-transcriptionally regulated in Th17 cells is unknown. Here, using RNA-binding protein HuR conditional knock-out (KO) and wild-type (WT) mice, we present evidence that HuR post-transcriptionally regulates CCR6 expression by binding to and stabilizing mRNA and by promoting CCR6 translation. We also found that HuR down-regulates several microRNA expressions, which could target the 3'-UTR of Ccr6 mRNA for decay. Accordingly, knock-out of HuR reduced CCR6 expression on Th17 cells and impaired their migration to CNS compared with the response of WT Th17 cells and thereby ameliorated EAE. Together, these findings highlight how HuR contributes to Th17 cell-mediated autoimmune neuroinflammation and support the notion that targeting HuR might be a potential therapeutic intervention for managing autoimmune disorders of the CNS.

show abstract

Cooperative interplay of let-7 mimic and HuR with MYC RNA

Cited by 19 publications

References 19 publications

Biogenesis and regulation of the let-7 miRNAs and their functional implications

Biogenesis and regulation of the let-7 miRNAs and their functional implications

Connections between 3′ end processing and DNA damage response: Ten years later

The RNA-binding protein HuR contributes to neuroinflammation by promoting C-C chemokine receptor 6 (CCR6) expression on Th17 cells

Contact Info

Product

Resources

About