Anti-tumoral Effects of miR-3189-3p in Glioblastoma

Jeansonne, Duane; DeLuca, Mariacristina; Marrero, Luis; Lassak, Adam; Pacifici, Marco; Wyczechowska, Dorota; Wilk, Anna; Reiss, Krzysztof; Peruzzi, Francesca

doi:10.1074/jbc.m114.633081

Cited by 29 publications

(26 citation statements)

References 33 publications

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“…Another example of an miRNA that amplifies the expression of its host gene is miR‐3189, which is located within an intron of the p53‐target gene GDF15 . This miRNA was found to activate p53 by targeting several of its inhibitors, but also to activate several of p53 target genes‐including GDF15‐ in a manner that was independent of the function of the transcription factor . Another interesting case involves an HSM member of the miR‐548 family located within an intron of the FHIT tumor‐suppressor and contributes to the anti‐neoplastic functions of its host gene .…”

Section: How Do Interactions Between Hsm/psm and Cancer Genes Emerge?mentioning

confidence: 99%

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Koufaris

2016

BioEssays

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The largest proportion of microRNAs in humans (ca. 40-50%) originated in the phylogenetic grouping defined as primates. The dynamic evolution of this family of non-coding RNA is further demonstrated by the presence of microRNA unique to the human species. Investigations into the role of microRNA in cancer have until recently mainly focused on the more ancient members of this RNA family that are widely conserved in the animal kingdom. As I describe in this review the evolutionary young lineage and species-specific microRNA could be important contributors to cancers, especially in particular organs in primates compared to more distantly-related research models. Elucidating the biological significance of primate and human-specific microRNA in cancer could have important implications for cancer research and the use of non-primate animal models.

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Section: How Do Interactions Between Hsm/psm and Cancer Genes Emerge?mentioning

confidence: 99%

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Koufaris

2016

BioEssays

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“…Similar to the upregulated miRNAs in serum, these miRNAs are largely unstudied in the liver. However, previously published data identifies miR-412 as upregulated in patients with ischemic hepatitis and patients with acetaminophen hepatotoxicity; miR-640 decreases angiogenesis in endothelial cells; miR-1537 is decreased in neuroblastoma; and miR-3189 plays an anti-tumoral role during glioblastoma [43-46]. Similar to the above miRNAs, miR-1537 and miR-3189 may act as tumor suppressors, which explains why they are upregulated in PSC alone patients versus CCA complicating PSC patients.…”

Section: Primary Sclerosing Cholangitismentioning

confidence: 99%

Diagnostic and therapeutic potentials of microRNAs in cholangiopathies

et al. 2017

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Cholangiopathies are a group of rare, devastating diseases that arise from damaged cholangiocytes, the cells that line the intra- and extra-hepatic bile ducts of the biliary epithelium. Cholangiopathies result in significant morbidity and mortality and are a major cause of liver transplantation. A better understanding of the underlying pathogenesis that influences cholangiocyte dysregulation and cholangiopathy progression is necessary, considering the dismal prognosis associated with these diseases. MicroRNAs are a class of small, non-coding RNAs that regulate post-transcriptional mRNA expression of specific genes. The role of microRNAs has expanded to include the initiation and development of many diseases, including cholangiopathies. Understanding microRNA regulation of cholangiopathies may provide diagnostic and therapeutic benefit for these diseases. In this review, the authors primarily focus on studies published within the last five years that help determine the diagnostic and therapeutic potential of microRNAs in cholangiopathies.

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“…RNA-binding Protein Immunoprecipitation-The RNAbinding protein immunoprecipitation Tat-IP was performed essentially as described previously (44). Briefly, cells were lysed in a lysis buffer consisting of 150 mM KCl, 25 mM Tris-HCl, pH 7.4, 5 mM EDTA, 0.5% Nonidet P-40, and 5 mM DTT and supplemented with 10 mM protease inhibitor mixture, 10 mM PMSF, 10 mM phosphatase inhibitor, 10 mM Na 3 VO 4 , and 100 units/ml RNase inhibitor (Applied Biosystems, Carlsbad, CA).…”

Section: Methodsmentioning

confidence: 99%

“…6G). To test whether Tat associates with TAU RNA, we performed Tat-RNA immunoprecipitation following our protocol (44). In this experiment, pEYFP-Tat (Tat), Myc-SC35 (SC35), and TAU minigene (Tau) were transfected into 293T cells with the following combinations: Tat ϩ TAU (sample 1); Tat alone (sample 2); SC35 ϩ Tat ϩ TAU (sample 3); and Tat ϩ SC35 (sample 4).…”

Section: Tau 3r Isoforms Are Increased and Sc35 Is Dysregulated In Humentioning

confidence: 99%

HIV-1-Tat Protein Inhibits SC35-mediated Tau Exon 10 Inclusion through Up-regulation of DYRK1A Kinase

Kadri

Pacifici

Wilk

et al. 2015

Journal of Biological Chemistry

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The HIV-1 transactivator protein Tat is implicated in the neuronal damage that contributes to neurocognitive impairment affecting people living with HIV/AIDS. Aberrant splicing of TAU exon 10 results in tauopathies characterized by alterations in the proportion of TAU isoforms containing three (3R) or four (4R) microtubule-binding repeats. The splicing factor SC35/ SRSF2 binds to nuclear RNA and facilitates the incorporation of exon 10 in the TAU molecule. Here, we utilized clinical samples, an animal model, and neuronal cell cultures and found that Tat promotes TAU 3R up-regulation through increased levels of phosphorylated SC35, which is retained in nuclear speckles. This mechanism involved Tat-mediated increased expression of DYRK1A and was prevented by DYRK1A silencing. In addition, we found that Tat associates with TAU RNA, further demonstrating that Tat interferes with host RNA metabolism in the absence of viral infection. Altogether, our data unravel a novel mechanism of Tat-mediated neuronal toxicity through dysregulation of the SC35-dependent alternative splicing of TAU exon 10. Furthermore, the increased immunostaining of DYRK1A in HIV؉ brains without pathology points at dysregulation of DYRK1A as an early event in the neuronal complications of HIV infection.

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Anti-tumoral Effects of miR-3189-3p in Glioblastoma

Abstract: Background: miR-3189-3p is a putative mirtron of growth differentiation factor 15 (GDF15). Results: MiR-3189-3p is down-regulated in glial tumors. Conclusion: MiR-3189-3p has tumor suppressor activities in glioblastoma cells. Significance: MiR-3189-3p has potential therapeutic properties.

Cited by 29 publications

References 33 publications

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Diagnostic and therapeutic potentials of microRNAs in cholangiopathies

HIV-1-Tat Protein Inhibits SC35-mediated Tau Exon 10 Inclusion through Up-regulation of DYRK1A Kinase

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