Two new miR‐16 targets: caprin‐1 and HMGA1, proteins implicated in cell proliferation

Kaddar, Tagrid; Rouault, Jean‐Pierre; Chien, Wu Chien; Chebel, Amel; Gadoux, Mylène; Salles, Gilles; Ffrench, Martine; Magaud, Jean‐Pierre

doi:10.1042/bc20080213

Cited by 77 publications

(59 citation statements)

References 38 publications

(65 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, it is noteworthy that these five miRNAs were associated by the web system to 57 cellular processes, including those in which HMGA proteins have been previously demonstrated to be involved, such as cell proliferation, differentiation, DNA-repair, chromatin modification and regulation of transcription (Fusco and Fedele, 2007;. The direct targeting of HMGA1 by miR-16 (Kaddar et al, 2009), and of HMGA2 by Let-7a (Lee and Dutta, 2007) and miR196ab (De Martino et al, 2009a) was previously reported. Moreover, previous studies showed that miR-26a regulates HMGA2 expression (Lee et al, 2011).…”

Section: Identification Of Hmga-targeting Mirnasmentioning

confidence: 99%

Downregulation of HMGA-targeting microRNAs has a critical role in human pituitary tumorigenesis

et al. 2011

View full text Add to dashboard Cite

Previous studies have demonstrated that high mobility group A proteins have a critical role on the onset of human pituitary adenomas. Indeed, both high mobility group A (HMGA) genes are overexpressed in pituitary adenomas, and consistently transgenic mice overexpressing either the Hmga1 or the Hmga2 gene develop mixed growth hormone/prolactin (GH-PRL)-secreting pituitary adenomas. Trisomy of chromosome 12, where HMGA2 is located, and/or amplification of the HMGA2 gene locus account for the HMGA2 overexpression in most human prolactinomas. Conversely, HMGA1 overexpression is not associated to any rearrangement or amplification of the HMGA1 locus. We have first identified micro RNAs (miRNAs) able to target both HMGA1 and HMGA2 messenger RNAs. Then, all of these miRNAs have been found downregulated in pituitary adenomas of different histotypes, compared with normal pituitary. Interestingly, their downregulation was also observed in nonfunctioning pituitary adenomas where HMGA2 overexpression is not associated to any alteration of the HMGA2 locus. Functional studies show that all these HMGA-targeting miRNAs inhibit the proliferation of the rat pituitary adenoma cell line GH3. Therefore, these results indicate that the downregulation of the miRNAs able to target the HMGA genes could contribute to increase HMGA protein levels in human pituitary adenomas, and then to pituitary tumorigenesis.

show abstract

Section: Identification Of Hmga-targeting Mirnasmentioning

confidence: 99%

Downregulation of HMGA-targeting microRNAs has a critical role in human pituitary tumorigenesis

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Loading equality was assessed by Ponceau red staining analysis and quantification of b-actin or a non-specific protein band (Wang et al, 2005;Kaddar et al, 2009). Quantifications were carried out by densitometric analysis using Kodak 1D Image Analysis Software (Sigma) as previously described (Baghdassarian et al, 1998).…”

Section: Western Blotmentioning

confidence: 99%

“…The half-life of the CDK1 protein was calculated according to the formula: T½ ¼ 0.3t/log(D1/D2), where D1 and D2 correspond to the protein levels at two different times and t is the corresponding interval of time microRNA quantification and microRNA arrays The total RNA was isolated as previously described. The expression levels of reference gene RNU48 as well as mature miR-16, miR-410 and miR-650 were analyzed as previously described (Kaddar et al, 2009) using TaqMan MicroRNA Assays (Applied Biosystems) by RT-qPCR, performed with the Applied Biosystems 7900 Sequence Detection system according to the manufacturer's instructions. According to the RT-PCR efficiency, 15 ng of total RNA was used for RNU48, miR-16 and miR-650 expression assays, whereas 50 ng was used for miR-410 (Supplementary Figure 5).…”

mentioning

confidence: 99%

Cyclin-dependent kinase 1 expression is inhibited by p16INK4a at the post-transcriptional level through the microRNA pathway

Domenech

Catallo

et al. 2010

Oncogene

View full text Add to dashboard Cite

The p16INK4a protein regulates cell cycle progression mainly by inhibiting the activity of G1-phase cyclin-dependent kinases (CDKs) 4 and 6, the subsequent retinoblastoma protein (pRb) phosphorylation and E2F transcription factor release. The p16INK4a protein can also repress the activity of other transcription factors, such as c-myc, nuclear factorkappaB and c-Jun/AP1. Here, we report that, in two p16WT and p53 WT cell lines (MCF7 and U87), p16INK4a overexpression induces a dramatic decrease in CDK1 protein expression. In response to p16 INK4a, the decreased rate of CDK1 protein synthesis, its unchanged protein half-life, unreduced CDK1 mRNA steady-state levels and mRNA half-life allow us to hypothesize that p16INK4a could regulate CDK1 expression at the post-transcriptional level. This CDK1 downregulation is mediated by the 3 0 -untranslated region (3 0 UTR) of CDK1 mRNA as shown by translational inhibition in luciferase assays and is associated with a modified expression balance of microRNAs (miRNAs) that potentially regulate CDK1, analyzed by TaqMan Human microRNA Array. The p16 INK4a-induced expression of two miRNAs (miR-410 and miR-650 chosen as an example) in MCF7 cells is confirmed by individual reverse transcriptionqPCR. Furthermore, we show the interaction of miR-410 or miR-650 with CDK1-3 0 UTR by luciferase assays. Endogenous CDK1 expression decreases upon both miRNA overexpression and increases with their simultaneous inhibition. The induction of miR-410, but not miR-650 could be related to the pRb/E2F pathway. These results demonstrate the post-transcriptional inhibition of CDK1 by p16 INK4a . We suggest that p16INK4a may regulate gene expression by modifying the functional equilibrium of transcription factors and consequently the expression balance of miRNAs.

show abstract

“…Caprin-1 mRNA is a target of the microRNAs miR-223 and miR-16 (Kaddar et al, 2009;Gong et al, 2013). In a study on the expression of Caprin-1 and miR-223 in several breast cancer cells and normal breast cells, miR-223 expression levels were significantly lower in cancer cells than in normal cells, while Caprin-1 expression was higher in cancer cells than in normal cells (Gong et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Bacterial expression and preliminary crystallographic studies of a 149-residue fragment of human Caprin-1

Zhu

Huang

et al. 2015

Acta Cryst Sect F

View full text Add to dashboard Cite

Caprin-1 is an RNA-binding protein which plays critical roles in several important biological processes, including cellular proliferation, the interferonmediated antiviral innate immune response, the maintenance of synaptic plasticity and the formation of RNA stress granules. Caprin-1 has been implicated in the pathogenesis of several human diseases, including osteosarcoma, breast cancer, viral infections, hearing loss and neurodegenerative disorders. Despite the emerging biological and physiopathological significance of Caprin-1, no structural information is available for this protein. Moreover, Caprin-1 does not have sequence similarity to any other protein with a known structure. It is therefore expected that structural studies will play a particularly crucial role in revealing the functional mechanisms of Caprin-1. Here, a protein fragment of human Caprin-1 consisting of residues 112-260 was expressed, purified and crystallized. Native and Se-SAD data sets were collected to resolutions to 2.05 and 2.65 Å , respectively, in different space groups.

show abstract

Two new miR‐16 targets: caprin‐1 and HMGA1, proteins implicated in cell proliferation

Cited by 77 publications

References 38 publications

Downregulation of HMGA-targeting microRNAs has a critical role in human pituitary tumorigenesis

Downregulation of HMGA-targeting microRNAs has a critical role in human pituitary tumorigenesis

Cyclin-dependent kinase 1 expression is inhibited by p16INK4a at the post-transcriptional level through the microRNA pathway

Bacterial expression and preliminary crystallographic studies of a 149-residue fragment of human Caprin-1

Contact Info

Product

Resources

About