Relevant bibliographies by topics / Let-7 miRNA

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Academic literature on the topic 'Let-7 miRNA'

Author: Grafiati
Published: 28 February 2024

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Journal articles on the topic "Let-7 miRNA"

1

Manier, Salomon, Antonio Sacco, Patricia Maiso, Yong Zhang, Yang Liu, Yosra Aljawai, Weixin Wang, et al. "Let-7 Microrna Family Members Regulate Cell Proliferation in Multiple Myeloma." Blood 120, no. 21 (November 16, 2012): 570. http://dx.doi.org/10.1182/blood.v120.21.570.570.

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Abstract Abstract 570 Background. MicroRNAs (miRNAs) play a pivotal role in tumorigenesis, due to their ability to target mRNAs involved in the regulation of cell proliferation, survival and differentiation. In particular, the Let-7 miRNA family members have been described to act as tumor suppressors, as demonstrated both in solid cancer and hematologic malignancies. However, the role of Let-7 in multiple myeloma (MM) has not been studied. Method. Circulating miRNA profiling has been performed in MM patients compared to healthy individuals using TaqMan human miRNA profiling, and validated by qRT-PCR. Exosomes were collected from both normal and MM peripheral blood, using ultracentrifugation; and further studied by using electron microscopy and immunogold labeling for the detection of CD63 and CD81. Exosomes were then evaluated for their miRNA content, by qRT-PCR. Gain- and loss-of functions studies were performed on MM cell lines (MM.1S; U266), using Let-7-mimic and Lin28B siRNA, respectively. Scramble probe-transfected cells were used as control. Cell proliferation and cell survival have been evaluated by using BrdU assay and MTT assay, respectively. Effects of Let-7 and Lin28B on signaling cascades have been evaluated by western blot. Results. We identified a MM specific signature characterized by down-regulation of miRNA-15a, −19b, −21, let-7b, let-7c and over-expression of miR-720 (P < 0.001). Circulating exosomes were studied at ultrastructural level showing positivity for CD81 and CD63, as demonstrated by immunogold labeling and electron microscopy. The same miRNA signature was found in the circulating exosomes, suggesting that circulating miRNAs may be transported by exosomes. The Let-7 family members were significantly decreased in peripheral blood of MM patient compared to healthy individuals, suggesting that Let-7 family could be down-regulated in MM cells. We then performed qRT-PCR in MM primary cells; and found that the Let-7 family is significantly down-regulated in MM primary cells, especially for Let-7b and c (5 fold change, P< 0.05). Over-expression of Let-7b and Let-7c in MM cells (U266; MM1S) transfected decreased cell proliferation. The RNA binding protein Lin28B is known to regulate the Let-7 family: we therefore performed Lin28-loss of function studies which led to up-regulation of the Let-7 family members, in MM transfected cells; and found that Lin28B-knockdown cells presented with reduced cell proliferation, supported by down-regulation of c-Myc and K-Ras, known to be Let-7-related targets. Conclusion. This data indicate that Let-7 miRNA family members play an important role in modulating MM biology, thus providing the basis for the development of new miRNA-based target therapies and biomarker in this disease. Disclosures: Ghobrial: Novartis: advisory board, advisory board Other; Millennium: Membership on an entity's Board of Directors or advisory committees; Onyx: Membership on an entity's Board of Directors or advisory committees; Bristol-Myers Squibb: advisory board, advisory board Other.
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Fang, W.-J., C.-Z. Lin, H.-H. Zhang, J. Qian, L. Zhong, and N. Xu. "Detection of let-7a MicroRNA by Real-time PCR in Colorectal Cancer: a Single-centre Experience from China." Journal of International Medical Research 35, no. 5 (September 2007): 716–23. http://dx.doi.org/10.1177/147323000703500518.

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Colorectal cancer, a heterogeneous disease arising from a complex series of molecular changes, is one of the world's leading causes of cancer deaths. MicroRNAs (miRNAs), an extensive class of small non-coding RNAs, have been implicated in cancer development and progression. One of the first miRNAs to be identified was let-7 miRNA, which has recently been found to be expressed at reduced levels in human lung cancer cells. We used a rapid stem-loop reverse transcription polymerase chain reaction method to quantify human let-7a miRNA expression in samples of human colorectal cancer. This method was able to detect let-7a miRNA in as little as 0.05 ng of total RNA from colorectal mucosa and its specificity was high (100%). Our results showed that the expression of let-7a miRNA was considerably reduced in two of eight patients. To our knowledge, this is the first study of Chinese patients to show reduced expression of endogenous let-7 miRNA in colorectal cancer.
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Campbell, Ashley M., Carlos F. De La Cruz-Herrera, Edyta Marcon, Jack Greenblatt, and Lori Frappier. "Epstein-Barr Virus BGLF2 commandeers RISC to interfere with cellular miRNA function." PLOS Pathogens 18, no. 1 (January 10, 2022): e1010235. http://dx.doi.org/10.1371/journal.ppat.1010235.

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The Epstein-Barr virus (EBV) BGLF2 protein is a tegument protein with multiple effects on the cellular environment, including induction of SUMOylation of cellular proteins. Using affinity-purification coupled to mass-spectrometry, we identified the miRNA-Induced Silencing Complex (RISC), essential for miRNA function, as a top interactor of BGLF2. We confirmed BGLF2 interaction with the Ago2 and TNRC6 components of RISC in multiple cell lines and their co-localization in cytoplasmic bodies that also contain the stress granule marker G3BP1. In addition, BGLF2 expression led to the loss of processing bodies in multiple cell types, suggesting disruption of RISC function in mRNA regulation. Consistent with this observation, BGLF2 disrupted Ago2 association with multiple miRNAs. Using let-7 miRNAs as a model, we tested the hypothesis that BGLF2 interfered with the function of RISC in miRNA-mediated mRNA silencing. Using multiple reporter constructs with 3’UTRs containing let-7a regulated sites, we showed that BGLF2 inhibited let-7a miRNA activity dependent on these 3’UTRs, including those from SUMO transcripts which are known to be regulated by let-7 miRNAs. In keeping with these results, we showed that BGLF2 increased the cellular level of unconjugated SUMO proteins without affecting the level of SUMO transcripts. Such an increase in free SUMO is known to drive SUMOylation and would account for the effect of BGLF2 in inducing SUMOylation. We further showed that BGLF2 expression inhibited the loading of let-7 miRNAs into Ago2 proteins, and conversely, that lytic infection with EBV lacking BGLF2 resulted in increased interaction of let-7a and SUMO transcripts with Ago2, relative to WT EBV infection. Therefore, we have identified a novel role for BGLF2 as a miRNA regulator and shown that one outcome of this activity is the dysregulation of SUMO transcripts that leads to increased levels of free SUMO proteins and SUMOylation.
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Pasquinelli, Amy E. "The primary target of let-7 microRNA." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 821–24. http://dx.doi.org/10.1042/bst20130020.

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The let-7 miRNA (microRNA) is an essential regulator of development from nematode worms to humans. Altered expression of let-7 results in larval arrest or lethality in Caenorhabditis elegans. Likewise, under- or over-expression of let-7 in human cells can result in cellular overproliferation or halted cell division respectively. Thus the biogenesis of this critical miRNA is controlled at multiple levels. An unexpected mechanism for regulating the initial processing of let-7 was recently found to involve the let-7 miRNA itself. The mature let-7 miRNA along with its effector protein, Argonaute, were shown to bind to a site in the primary transcripts produced by the let-7 gene. This interaction enhances processing through a novel auto-regulatory feedback loop. This discovery highlights a new role for the miRNA complex in regulating miRNA biogenesis and enriches the classes of RNAs targeted by Argonaute.
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Ren, Zhiji, and Victor R. Ambros. "Caenorhabditis elegans microRNAs of the let-7 family act in innate immune response circuits and confer robust developmental timing against pathogen stress." Proceedings of the National Academy of Sciences 112, no. 18 (April 20, 2015): E2366—E2375. http://dx.doi.org/10.1073/pnas.1422858112.

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Animals maintain their developmental robustness against natural stresses through numerous regulatory mechanisms, including the posttranscriptional regulation of gene expression by microRNAs (miRNAs). Caenorhabditis elegans miRNAs of the let-7 family (let-7-Fam) function semiredundantly to confer robust stage specificity of cell fates in the hypodermal seam cell lineages. Here, we show reciprocal regulatory interactions between let-7-Fam miRNAs and the innate immune response pathway in C. elegans. Upon infection of C. elegans larvae with the opportunistic human pathogen Pseudomonas aeruginosa, the developmental timing defects of certain let-7-Fam miRNA mutants are enhanced. This enhancement is mediated by the p38 MAPK innate immune pathway acting in opposition to let-7-Fam miRNA activity, possibly via the downstream Activating Transcription Factor-7 (ATF-7). Furthermore, let-7-Fam miRNAs appear to exert negative regulation on the worm’s resistance to P. aeruginosa infection. Our results show that the inhibition of pathogen resistance by let-7 involves downstream heterochronic genes and the p38 MAPK pathway. These findings suggest that let-7-Fam miRNAs are integrated into innate immunity gene regulatory networks, such that this family of miRNAs modulates immune responses while also ensuring robust timing of developmental events under pathogen stress.
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Liu, Jun, Madeline A. Sauer, Shaza G. Hussein, Junyu Yang, Daniel G. Tenen, and Li Chai. "SALL4 and microRNA: The Role of Let-7." Genes 12, no. 9 (August 24, 2021): 1301. http://dx.doi.org/10.3390/genes12091301.

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SALL4 is a zinc finger transcription factor that belongs to the spalt-like (SALL) gene family. It plays important roles in the maintenance of self-renewal and pluripotency of embryonic stem cells, and its expression is repressed in most adult organs. SALL4 re-expression has been observed in different types of human cancers, and dysregulation of SALL4 contributes to the pathogenesis, metastasis, and even drug resistance of multiple cancer types. Surprisingly, little is known regarding how SALL4 expression is controlled, but recently microRNAs (miRNAs) have emerged as important regulators of SALL4. Due to the ability of regulating targets differentially in specific tissues, and recent advances in systemic and organ specific miRNA delivery mechanisms, miRNAs have emerged as promising therapeutic targets for cancer treatment. In this review, we summarize current knowledge of the interaction between SALL4 and miRNAs in mammalian development and cancer, paying particular attention to the emerging roles of the Let-7/Lin28 axis. In addition, we discuss the therapeutic prospects of targeting SALL4 using miRNA-based strategies, with a focus on the Let-7/LIN28 axis.
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Zhang, Pengcheng, Mallory I. Frederick, and Ilka U. Heinemann. "Terminal Uridylyltransferases TUT4/7 Regulate microRNA and mRNA Homeostasis." Cells 11, no. 23 (November 23, 2022): 3742. http://dx.doi.org/10.3390/cells11233742.

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The terminal nucleotidyltransferases TUT4 and TUT7 (TUT4/7) regulate miRNA and mRNA stability by 3′ end uridylation. In humans, TUT4/7 polyuridylates both mRNA and pre-miRNA, leading to degradation by the U-specific exonuclease DIS3L2. We investigate the role of uridylation-dependent decay in maintaining the transcriptome by transcriptionally profiling TUT4/7 deleted cells. We found that while the disruption of TUT4/7 expression increases the abundance of a variety of miRNAs, the let-7 family of miRNAs is the most impacted. Eight let-7 family miRNAs were increased in abundance in TUT4/7 deleted cells, and many let-7 mRNA targets are decreased in abundance. The mRNAs with increased abundance in the deletion strain are potential direct targets of TUT4/7, with transcripts coding for proteins involved in cellular stress response, rRNA processing, ribonucleoprotein complex biogenesis, cell–cell signaling, and regulation of metabolic processes most affected in the TUT4/7 knockout cells. We found that TUT4/7 indirectly control oncogenic signaling via the miRNA let-7a, which regulates AKT phosphorylation status. Finally, we find that, similar to fission yeast, the disruption of uridylation-dependent decay leads to major rearrangements of the transcriptome and reduces cell proliferation and adhesion.
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Medhi, Ragini, Jonathan Price, Giulia Furlan, Beronia Gorges, Alexandra Sapetschnig, and Eric A. Miska. "RNA uridyl transferases TUT4/7 differentially regulate miRNA variants depending on the cancer cell type." RNA 28, no. 3 (December 23, 2021): 353–70. http://dx.doi.org/10.1261/rna.078976.121.

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The human terminal uridyl transferases TUT4 and TUT7 (TUT4/7) catalyze the additions of uridines at the 3′ end of RNAs, including the precursors of the tumor suppressor miRNA let-7 upon recruitment by the oncoprotein LIN28A. As a consequence, let-7 family miRNAs are down-regulated. Disruption of this TUT4/7 activity inhibits tumorigenesis. Hence, targeting TUT4/7 could be a potential anticancer therapy. In this study, we investigate TUT4/7-mediated RNA regulation in two cancer cell lines by establishing catalytic knockout models. Upon TUT4/7 mutation, we observe a significant reduction in miRNA uridylation, which results in defects in cancer cell properties such as cell proliferation and migration. With the loss of TUT4/7-mediated miRNA uridylation, the uridylated miRNA variants are replaced by adenylated isomiRs. Changes in miRNA modification profiles are accompanied by deregulation of expression levels in specific cases. Unlike let-7s, most miRNAs do not depend on LIN28A for TUT4/7-mediated regulation. Additionally, we identify TUT4/7-regulated cell-type-specific miRNA clusters and deregulation in their corresponding mRNA targets. Expression levels of miR-200c-3p and miR-141-3p are regulated by TUT4/7 in a cancer cell-type-specific manner. Subsequently, BCL2, which is a well-established target of miR-200c is up-regulated. Therefore, TUT4/7 loss causes deregulation of miRNA–mRNA networks in a cell-type-specific manner. Understanding of the underlying biology of such cell-type-specific deregulation will be an important aspect of targeting TUT4/7 for potential cancer therapies.
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Emmrich, Stephan, Sarva Keihani, Dirk Reinhardt, and Jan-Henning Klusmann. "Members of the Mir-99/100~125 Tricistrons Cooperatively Induce a Pre-Leukemic Myeloproliferative Disorder." Blood 126, no. 23 (December 3, 2015): 3579. http://dx.doi.org/10.1182/blood.v126.23.3579.3579.

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Abstract MicroRNAs (miRNAs) reflect the best studied class of regulatory non-coding RNAs (ncRNAs), which control genetic networks with key cellular functions. In vertebrate genomes, a significant number of miRNA genes are located closely adjacent to each other in miRNA polycistrons. The mature miRNAs of the three human miR-99/100~125 clusters, each containing one miR-99/100, let-7 and miR-125 family member in identical polycistronic configuration, are processed from one single transcript and are highly expressed in acute promyelocytic leukemia (APL). Expression profiling by qPCR in sorted murine hematopoietic stem cells (HSCs), common myeloid progenitors (CMPs), megakaryocytic erythroid progenitors (MEPs) and granulocytic monocytic progenitors (GMPs) revealed high expression levels of miR-99/100 and miR-125 family members in HSCs and CMPs. However, the consequences of the coordinated expression of the miRNAs belonging to different seed families on self-renewal and proliferation of HSCs and myeloid progenitors and their contribution to the pathogenesis of APL are not well understood. To elucidate the genetic interactive network of miR-99/100~125 miRNAs and the role of each individual miRNA within this network, we generated a set of eight different constructs covering any permutation of miRNA family members from the two miR-99/100~125 clusters on hsa11 and hsa21 (miR-99a, miR-125b-2, let-7c, miR-99a/let-7c, miR-100/miR-125b-1, let-7a-2/miR-125b-1, miR-100/let-7a-2/miR-125b-1 and miR-99a/let-7c/miR-125b-2). Lentiviral overexpression of these constructs in human hematopoietic stem and progenitor cells (HSPCs) resulted in a significant reduction of monocytic/macrophage colony-forming units (CFU-M; 2.2-2.8-fold, p≤0.05) and granulocytic CFU-Gs (2-4.3-fold, p≤0.05) in methylcellulose-based CFU assays exclusively for miR-125-containing bi-/tricistronic constructs (miR-100/miR-125b-1, let-7a-2/miR-125b-1, miR-100/let-7a-2/miR-125b-1 and miR-99a/let-7c/miR-125b-2), but not for the single miRNA expression constructs. Accordingly, during myelomonocytic differentiation HSPCs transduced with those miR-125-containing bi-/tricistronic constructs gave rise to a major population of monomorphic, non-adherent cells devoid of granulocytic and monocytic markers, which was not present in single miRNA-transduced cells. In murine isogenic transplantation experiments (N=105), only the combined miRNA expression of miR-125b with let-7 and/or miR-99/100 led to the expansion and retention of immature Gr-1(low)/Mac-1(+)/B220(-) cells in the bone marrow (1.6-1.8fold; p≤0.01). Accordingly, either the CMP or GMP compartment of transplanted mice was expanded in miR-125-containing bi-/tricistronic constructs (CMPs 1.6-fold in let-7a-2/miR-125b-1, GMPs 1.8-1.9-fold in miR-100/miR-125b-1 and tricistrons; p≤0.01;), but not upon single miRNA overexpression (1.1-1.3-fold; p≥0.1). Global gene expression profiling of human HSPCs transduced with the eight miRNA constructs revealed a core expression signature commonly regulated by the four miR-125b-containing bi-/ tricistronic constructs (367 genes upregulated [>1.5-fold]; 417 genes downregulated). Strikingly, this core signature is enriched for genes with concordant expression in leukemic stem cells (LSCs) and HSCs (FDR q≤1.8x10-14). The genes of the core signature were not or only modestly affected in the context of the single miRNAs. Thus, the miR-99/100~125 tricistron miRNAs form an interaction network, wherein the combined activity of miR-125b with let-7 and/or miR-99/100 family members converged to induce a stem cell signature creating a synthetic phenotype. The synthetic phenotype can only be observed in the combination of two or all three miRNAs but not for each miRNA alone, and is generated by miR-99/100 and/or let-7 altering the hematologically dominant miR-125 phenotype. This interactive network might explain the genomic miR-99/100~125 clustering and reveals a novel cooperative mode to induce self-renewal and a differentiation block in myeloid progenitor cells, predisposing them to leukemic transformation in APL. Disclosures No relevant conflicts of interest to declare.
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de Vasconcellos, Jaira F., Colleen Byrnes, Y. Terry Lee, Megha Kaushal, Joshua M. Allwardt, Antoinette Rabel, and Jeffery L. Miller. "Targeted Reduction of Let-7a miRNA Increases Fetal Hemoglobin in Human Adult Erythroblasts." Blood 124, no. 21 (December 6, 2014): 451. http://dx.doi.org/10.1182/blood.v124.21.451.451.

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Abstract MicroRNAs (miRNAs) are a class of small, noncoding RNAs that bind and regulate target messenger RNAs (mRNAs). The let-7 family consists of twelve genes encoding nine highly conserved miRNAs that are involved in developmental timing events in multicellular organisms. Previous studies showed regulation during the fetal-to-adult transition in the erythroid lineage with significant increases in let-7 miRNAs from adult compared to umbilical cord blood reticulocytes (1). Further studies indicated that reduced expression of let-7 in adult CD34+ cells by “sponge” targeting the miRNA family seed region caused increased fetal hemoglobin (HbF), but the mean level of HbF remained less than 20% of the total hemoglobin (2). Increased expression of LIN28A (a major regulator of all let-7 miRNAs) caused greater increases in HbF (greater than 30% of the total) in cultured erythrocytes from pediatric patients with HbSS genotype (3). However, these studies did not address the potential for targeting an individual let-7 miRNA family member to regulate HbF expression. For this purpose, we initially determined the expression levels of mature let-7 family members in purified cell populations sorted from peripheral blood. The total levels of let-7 miRNAs in peripheral blood cells were as follows: reticulocytes: 1.7E+08 ± 1.0E+08 copies/ng; neutrophils: 2.0E+07 ± 1.1E+07 copies/ng; lymphocytes: 1.1E+07 ± 6.2E+06 copies/ng and monocytes: 3.5E+06 ± 2.7E+06 copies/ng. Among the individual species, let-7a was identified as a predominantly expressed let-7 family member in reticulocytes. As such, we hypothesized that specifically targeting let-7a may be sufficient to regulate HbF levels. To study the effects of let-7a miRNAs upon erythropoiesis and globin expression, a lentiviral construct that incorporated the tough decoy (TuD) design to target let-7a was compared with empty vector controls. Transductions were performed in CD34+ cells from five adult healthy volunteers cultivated ex vivo in erythropoietin-supplemented serum-free media for 21 days. Down-regulation of let-7a was confirmed by Q-RT-PCR at day 14 (control: 1.4E+07 ± 2.4E+06 copies/ng; let-7a-TuD: 1.6E+06 ± 4.6E+05 copies/ng; p=0.0003). Cell proliferation and differentiation were comparable in let-7a-TuD versus control transductions. Expression levels of globin genes were evaluated upon let-7a-TuD by Q-RT-PCR. Let-7a-TuD transductions caused significantly increased gamma-globin mRNA expression levels compared to control transductions (control: 1.2E+06 ± 6.8E+05 copies/ng; let-7a-TuD: 1.1E+07 ± 4.5E+06 copies/ng; p=0.004). HPLC analyses at the end of the culture period demonstrated robust increases in HbF levels after let-7a-TuD transduction (HbF control: 4.7 ± 0.6%; let-7a-TuD: 38.2 ± 3.8%; p=0.00003). In addition, the expression patterns of the erythroid transcription factors BCL11A, KLF1 and SOX6 were investigated. Let-7a-TuD decreased BCL11A mRNA expression levels (control: 1.7E+03 ± 4.5E+02 copies/ng; let-7a-TuD: 4.3E+02 ± 1.8E+02 copies/ng; p=0.003), but major changes in KLF1 or SOX6 were not detected. In summary, we report here that the let-7 miRNA family is differentially expressed in purified cell populations from adult human blood, and that let-7a is a predominantly expressed species in reticulocytes. Further, targeted reduction of let-7a in erythroblasts is sufficient to cause robust increases in gamma-globin mRNA expression and HbF to mean levels around 35-40% of the total hemoglobin produced. Targeting of individual let-7 genes or RNA transcripts may be useful for therapeutic induction of HbF expression in patients with sickle cell disease or other beta-hemoglobinopathies. 1) Noh SJ et al. J Transl Med. 7:98 (2009). 2) Lee YT et al. Blood. 122:1034-41 (2013). 3) Vasconcellos JF et al. Blood. 122: Abstract 313 (2013). Disclosures No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "Let-7 miRNA"

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ORNAGHI, SARA. "Modulazione dell'espressione del miRNA let-7 da parte del nuovo peptide pre-implantation factor: implicazioni per la neuroprotezione in un modello animale di encefalopatia ipossico-ischemica del prematuro." Doctoral thesis, Universita' Milano Bicocca, 2014. http://hdl.handle.net/10281/193813.

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Leppert, Ulrike. "Die Biogenese des COP9 Signalosoms wird durch microRNAs der let-7-Familie reguliert." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16224.

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Das COP9 Signalosom ist ein hochkonservierter Proteinkomplex bestehend, aus acht Untereinheiten. In der vorgelegten Promotionsarbeit konnte ein bislang unbekannter Regulationsmechanismus der Biogenese des COP9 Signalosoms identifiziert werden. Die siRNA-vermittelte Reduktion der CSN1-Expression führte zu einer Reduktion der Expression aller CSN-Untereinheiten. Die Transfektion von His-CSN1 in siCSN1-Zellen induzierte die CSN-Neusynthese und ferner einen Anstieg der c-Myc- und STAT1 Expression. Durch die Stimulation der Zellen mit IFN alpha bzw. IFN gamma konnte die de novo Synthese des CSN-Komplexes induziert werden. Die siRNA-vermittelte Inhibition von STAT1, c-Myc bzw. Lin28B führte ebenso wie die Behandlung der Zellen mit AG9 bzw. AG490, pharmakologischen Inhibitoren der JAK-Kinasen, zu einer Reduktion der Proteinexpression der CSN-Untereinheiten. Dabei standen signifikanten Veränderungen auf der Proteinebene geringfügige Änderungen auf der mRNA-Ebene gegenüber. Daher wurde ein post-transkriptioneller Mechanismus zur Regulation der Expression der CSN-Untereinheiten unter Beteiligung von miRNAs postuliert. Diese Regulation wird vermutlich durch die Aktivität von c-Myc und Lin28B verstärkt. Dies stellt einen neuen, bislang unbekannten Mechanismus für die Regulation der Biogenese des COP9 Signalosoms, vermutlich über den c-Myc/Lin28B/let-7-Weg, dar. Die Co-Transfektion der siCSN1-Zellen mit spezifischen komplementären Inhibitoren dieser miRNAs führte zu einer Induktion der Proteinexpression der CSN-Untereinheiten. Die Transfektion von let-7 miRNA-Mimics bewirkte eine Reduktion der Expression der CSN-Untereinheiten in den siCSN1-Zellen. Ferner konnten im Rahmen dieser Arbeit mittels der miRBase Sanger Datenbank und der Software MicroInspector Bindestellen für let-7 miRNAs an den mRNAs der CSN- und der proteasomalen Lid-Untereinheiten identifiziert werden. Der gezeigte Regulationsmechanismus könnte auch für die Biogenese des proteasomalen Lids von Bedeutung sein.
The COP9 signalosome is a highly conserved protein complex composed of eight subunits. In this study a novel, regulatory mechanism of CSN biogenesis was identified. We used stable transfected siCSN1 cells in which the protein and the mRNA expression of CSN subuntis were downregulated. Transfection of His-CSN1 in those siCSN1 cells led to the induction of the de novo Synthesis of the whole CSN complex. In addition the expression of the transcription factors STAT1 and c-Myc was elevated. The cells were treated with IFN alpha or IFN gamma, respectively. This resulted in the induction of the CSN de novo synthesis. Moreover, the siRNA-mediated inhibition of STAT1, c-Myc, Lin28B as well as treatment with the pharmacological inhibitors AG9 or AG490 led to a reduced protein expression of the analysed CSN subunits. We found that in all experiments there was a significant change on protein level in contrast to a marginal change on the RNA level. Based on our study we hypothesized that the CSN biogenesis ist regulated post-transcriptionally by miRNAs. The participation of miRNAs in the regulation of CSN biogenesis was further analysed. The siCSN1 cells were transfected with complementary hairpin inhibitors of let-7 miRNAs, leading to an induction of the CSN synthesis. The transfection of let-7 miRNA-mimics, which enhance the impact of miRNA on target mRNAs, resulted in an decrease of the CSN expression. These findings prove the involvement of miRNAs in CSN biogenesis, presumably via the c-Myc/Lin28B/let-7 pathway. Furthermore, using miRBase Sanger database and MicroInspector software, potential binding sites for let-7 miRNAs were detected within the mRNA sequences of CSN subunits as well as of subunits of the proteasomal lid. Therefore, there is evidence to suggest that this mechanism is crucial for the regulation of the biogenesis of the proteasomal lid as well.
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Nouri, Sirine. "Development of new NMR methods to study miRNA dynamics." Electronic Thesis or Diss., Lyon 1, 2023. http://www.theses.fr/2023LYO10006.

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Les ARN non-codants ont été découverts au cours des dernières décennies et sont impliqués dans de nombreux processus biologiques. La compréhension des mécanismes qui permettent à ces ARN de remplir leur fonction est essentielle, tant au niveau fondamental que dans la perspective d’applications thérapeutiques. La Résonance Magnétique Nucléaire (RMN) des liquides est un outil d’analyse unique qui permet de caractériser la structure et la dynamique des ARN. L’objectif de cette thèse est le développement de nouvelles méthodes RMN pour décrire la dynamique complexe des ARN. Une attention particulière est portée sur le précurseur du micro ARN let-7, un système biologique intéressant car la dérégulation de let-7 pertube le développement et la différenciation cellulaire et conduit au développement de maladies cellulaires telles que le cancer. Cet ARN a une structure en tige et boucle. En raison de sa taille et de la flexibilité inhérente à sa grande boucle, l’étude de cet ARN par RMN est complexe et innovante. Dans un premier temps, ce manuscrit décrit la mise en place d’un protocole expérimental de production d’échantillons d’ARN hautement concentrés et très purs pour la RMN. Ensuite, une nouvelle stratégie d’attribution des spectres RMN est exposée. Elle s’applique aux ARN composés de grands éléments non structurés. Ces méthodes sont utilisées pour étudier la structure et la dynamique du précurseur du micro ARN let- 7. Des données expérimentales ont été mesurées sur cet ARN à partir de deux techniques analytiques : la diffusion de rayons X aux petits angles et la spectroscopie RMN (couplages dipolaires résiduels externes ou induits par le champ). Ces données expérimentales sont utilisées pour sélectionner un ensemble de conformations parmi une base de données générée par des simulations de dynamique moléculaire. L’ensemble sélectionné est choisi pour représenter au mieux les données expérimentales. À partir de l’analyse structurelle de cet ensemble de conformations et d’expériences RMN qui caractérisent des phénomènes d’échange lents au sein de l’ARN, nous avons pu proposer une hypothèse : la combinaison de transitions dynamiques rapides et lentes au sein de la grande boucle de l’ARN permet d’expliquer la capacité de cet ARN à interagir avec différentes protéines
Non-coding RNAs have appeared in the last decades as central elements of numerous biological processes and understanding how they can perform their function is essential both at the fundamental level and in the perspective of potential applications. Solution- state Nuclear Magnetic Resonance (NMR) methods are a unique way to characterize the structure and dynamics of RNAs and thus shed light on their intrinsic plasticity. This thesis focuses on the development of novel methodologies to describe complex dynamics occurring in RNA with a particular focus on the let-7 micro RNA precursor an interesting system as the deregulation of let-7 can perturb cell development and differentiation and lead to the development of cell-based diseases such as cancer. Due to its size and the flexibility inherent to large RNA loop, the study of the let-7 miRNA precursor remains at the forefront of biological NMR. This work addresses the implementation of an enzymatic production protocol of high concentrated and very pure RNA sample for NMR spectroscopy and the development of new strategies for resonance assignment of RNAs with large non-helical dynamic elements. These methods are used to investigate the structure and dynamics of the let-7 micro RNA precursor. A combination of Small-Angle X-Ray scattering and NMR spectroscopy experimental data (Residual Dipolar Couplings either externally or field-induced) were measured. These experimental data are used in an ensemble optimization method to selectively refine models generated by extensive all-atom molecular dynamics simulations. The selected ensemble is in good agreement with the NMR experimental data. From the structural analysis of the selected ensemble and Chemical Exchange Saturation Transfer experiments, we propose a hypothesis that correlates fast and slow exchange processes happening in the non-helical region of the RNA with its ability to interact with regulatory proteins
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Mayr, Florian [Verfasser]. "Structural and Functional Analysis of Lin28-Mediated Inhibition of let-7 miRNA Biogenesis / Florian Mayr." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1035182513/34.

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Wagner, Siegfried [Verfasser]. "Analyses of miRNA let-7 and its targets in canine neoplasias as model for human counterparts / Siegfried Wagner." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2015. http://d-nb.info/1070285471/34.

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Thornton, James Edward. "Roles for Terminal Uridyl Transferases in the Post-Transcriptional Regulation of Developmental miRNAs." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11195.

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MicroRNAs (miRNAs) are a diverse and evolutionarily conserved class of non-coding RNAs that play a multitude of roles in many branches of eukaryotic biology. The regulation of miRNAs is dynamically controlled both spatially and temporally, and the expression of miRNAs can be modulated at the level of transcription or at points downstream of the miRNA maturation process. A relevant example of post-transcriptional miRNA regulation is the blockade of let-7 precursor miRNAs by Lin28 in embryonic stem cells. This pathway, which is initiated by the small RNA-binding protein Lin28, recruits the terminal uridyl transferase (TUTase) Zcchc11 to add a non-templated oligouridine tail to the miRNAs 3' end, and signals it for degradation by the cytoplasmic exonuclease Dis3l2. The Lin28/let-7 axis is essential for development and metabolic homeostasis, and is reactivated in a subset of human cancers. This thesis describes the biochemical mechanism underlying Lin28-mediated degradation of let-7, as well as a novel role for Zcchc11 and the related TUTase Zcchc6 in targeting mature developmental miRNAs in a Lin28-independent manner.
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Anene, Chinedu A. "Platelet micro-particles induce angiogenesis through the delivery of the micro-RNA Let-7a into endothelial cells." Thesis, University of Bradford, 2017. http://hdl.handle.net/10454/16041.

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Cardiovascular disease is a major cause of morbidity and mortality around the globe, which is linked to athero-thrombosis. The risk factors for atherothrombosis, thus cardiovascular disease is impaired anti-thrombotic and antiinflammatory functions of the endothelium. Thrombosis is a hallmark of cardiovascular disease/complications characterised by increased platelet activation and increased secretion of platelet micro-particles that induce angiogenesis. This study determined the role of platelet micro-particles derived microRNA in the regulation of angiogenesis and migration, with a focus on the regulation of thrombospondin-1 release by platelet micro-particles delivered Let- 7a. The role of thrombospondin-1 receptors (integrin beta-1 and integrin associated protein) and downstream caspase-3 activation were explored by Let-7a inhibition prior to PMP treatment. MicroRNA dependent modulation of proangiogenic proteins including monocyte chemoattractant protein-1 and placental growth factor, and recruitment of activating transcription factor-4 protein to their promoter regions were explored. Main findings are: 1. Platelet micro-particles induce angiogenesis, migration, and release of novel cytokine subsets specific to platelet micro-particle’s RNA content. 2. The targeting of thrombospondin-1 mRNA by platelet micro-particles’ transferred Let-7a chiefly modulate the angiogenic effect on endothelial cells. 3. The inhibition of thrombospondin-1 translation enable platelet micro-particles to increase angiogenesis and migration in the presence of functional integrin beta-1 and integrin associated protein, and reduced cleaving of caspase-3. 4. Platelet micro-particle modulate the transcription of monocyte chemoattractant protein-1 and placental growth factor in a Let-7a dependent manner. 5. Let-7a induce angiogenesis ii independent of other platelet micro-particle’s microRNAs. Platelet micro-particle derived Let-7a is a master regulator of endothelial cell function in this model, which presents an opportunity for the development of new biomarkers and therapeutic approaches in the management of cardiovascular disease. Future studies should aim to confirm these findings in-vivo.
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Fu, Xiaonan. "Functional study of miRNA-mRNA interactions in malaria mosquito An. gambiae." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/96216.

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Female adults of many mosquito species possess distinct physiological features adapting to blood feeding for successful reproduction. The disease pathogens that are transmitted by mosquitoes have evolved to take advantages of the indispensable blood feedings to complete their transmission cycles and to survive attacks from the mosquito's innate immune system. Normal egg development and mosquito immunity are tightly controlled by tissue- and stage-specific gene expression and coordinated by many signal molecules in the mosquito. Understanding gene regulation affecting mosquito reproduction and malaria parasites infection is of paramount importance for developing novel malaria control strategies. A growing body of evidence indicates that microRNAs (miRNAs) are involved in egg maturation and immune reactions against invading pathogens in mosquitoes. However, the molecular mechanisms by which specific miRNAs selectively modulate reproduction and the survival of pathogens are largely unknown. The miRNA-induced gene-silencing pathway in mosquitoes was mostly extrapolated from the studies of flies. To explore the dynamics of miRNAs in reproduction, I used small RNAs sequencing to monitor miRNAs expression and their association with Argonaute 1 (Ago1) and Argonaute 2 (Ago2) in the malaria mosquito Anopheles gambiae (An. gambiae) during the 72-h period immediately after blood feeding. I found the abundance and Ago loading of most of the mature miRNAs were relatively stable after blood ingestion. However, miRNAs of the miR-309/286/2944 cluster were considerably upregulated after blood feeding. I confirmed that miR-309 is essential for normal egg development by depletion of endogenous miR-309 with a specific antagomir. In addition, my results showed that the Ago association of some miRNAs was not proportional to their cellular abundance implying additional regulation at miRNA integration. To investigate the functional roles of miRNAs and define context-dependent miRNA-mRNA interactions during the reproductive process, I have applied an innovative experimental approach to study miRNA-mRNA interactome. CLEAR (covalent ligation of endogenous Argonaute-bound RNAs)-CLIP can generate miRNA-mRNA chimeras from UV-irradiation stabilized Ago-miRNA-mRNA complex. My results have defined tens of thousands of miRNA-mRNA interactions in mosquitoes, including novel targets for mosquito-specific miRNAs. Verification of the predicted interactions using mRNA-seq, ribosome-profiling, and luciferase reporter assay revealed a reliable miRNA-mRNA interaction network. Based on the detected interactions, I refined the paring rules for mosquito miRNAs and illustrated the dynamic pairing between different regions of miRNAs with their targets in vivo. The miRNA-mRNA interactions were compared using this approach at multiple time points before and after blood feeding. Importantly, this study showed that the interactions were dynamic and enriched in genes that are involved in metabolisms, supporting the proposed functions of miRNAs in coordinating the gene regulation in mosquito reproduction. Plasmodium falciparum (P. falciparum) is a major human malaria parasite. To understand the functions of miRNAs in the mosquito resistance to Plasmodium infection, we analyzed the miRNA-mRNA interactions after female mosquitoes taking a P. falciparum-infected blood meal or an uninfected blood meal. Comparison of the interactions revealed enhanced miRNA-mRNA interactions after P. falciparum infection involving a group of immunity-related genes. In summary, this study has provided a systematic view and significantly advanced our understanding of the miRNA functions in mosquito reproduction and P. falciparum infection.
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Rößling, Rosa [Verfasser]. "Die let-7-miRNA-Familie: Untersuchung ihres Vorkommens in humanem Liquor bei neurodegenerativen Erkrankungen und ihrer neurotoxischen Wirkung in vitro / Rosa Rößling." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1223928578/34.

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König, Annekatrin [Verfasser], Halyna [Akademischer Betreuer] Shcherbata, Andreas [Akademischer Betreuer] Wodarz, and Jörg [Akademischer Betreuer] Großhans. "Ecdysone signaling and miRNA let-7 cooperate in regulating the differentiation of the germline stem cell progeny / Annekatrin König. Gutachter: Andreas Wodarz ; Jörg Großhans. Betreuer: Halyna Shcherbata." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2015. http://d-nb.info/1070686158/34.

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Book chapters on the topic "Let-7 miRNA"

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Skonieczna, Magdalena, Dorota Hudy, Patryk Bil, Malgorzata Adamiec, Marta Stachowska, and Krzysztof Biernacki. "Role of Let-7 Family miRNAs in Migration of Colorectal Cancer HCT 116 and Caco-2 Cells After Stimulation by the Adipokine Vaspin. Time-Lapse Live-Cell Microscopic Observations." In Advances in Intelligent Systems and Computing, 47–61. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29885-2_5.

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Zentilli, Marcos, Milton C. Graves, Ryan Mathur, Jacob J. Hanley, Larry M. Heaman, and Ricardo Boric. "Locating the “Missing Half” of the Giant Chuquicamata Porphyry Copper Deposit, Chile." In Tectonomagmatic Influences on Metallogeny and Hydrothermal Ore Deposits: A Tribute to Jeremy P. Richards (Volume I), 69–85. Society of Economic Geologists, 2021. http://dx.doi.org/10.5382/sp.24.05.

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Abstract The supergiant Chuquicamata porphyry Cu-Mo deposit in northern Chile is truncated on its west side by a N-S-trending regional fault (the West fault), juxtaposing its ore to a relatively barren granodiorite (Fortuna Igneous Complex). There has been much speculation about the fate of, and extensive exploration for, the “missing half” of the deposit. It has been proposed that the west side of the fault hides the ore at depth, or that it was uplifted and the ore eroded; however, regional geologic mapping suggests that the West fault had a postore left-lateral strike-slip displacement of ca. 35 km. Accordingly, exploration, so far unsuccessful, has been focused in an area 35 km south near the Loa River and the city of Calama. In 1989, the Mina Ministro Hales (MMH) deposit was unexpectedly discovered west of the fault, under thick gravels, only 7 km south of the main mine. A previous study at MMH had suggested that mineralization was as old as 39 Ma, hence its ores were correlated with deposits of that age near Calama. Our recent U-Pb and Re-Os dating indicates that MMH mineralization was formed between 35 and 31 Ma, thus concurrently with Chuqui. The geochemistry of host Triassic and Eocene porphyry intrusions, ore mineralogy, and common Pb isotope ratios of hypogene sulfides at MMH and Chuqui proper are indistinguishable. Fluid inclusion data for paragenetically early porphyry assemblages at MMH closely mimic Th-salinity data from earlier studies at Chuqui, showing little or no evidence of boiling but indicating widely fluctuating confining pressures, compatible with hydraulic fracturing and fault movement during and after mineralization at a minimum initial lithostatic constraint of 5- to 8-km depth. We propose that MMH is a sheared-off portion of Chuqui, wedged in a fault cymoid loop and spared the full 35-km displacement of the West fault.
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Conference papers on the topic "Let-7 miRNA"

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Powers, John T., Kaloyan Tsanov, Frederik Roels, Catherine Spina, Richard Ebright, Marc Seligson, Yvanka de Soysa, et al. "Abstract LB-165: Multiple mechanisms disrupt let-7 miRNA biogenesis and function in neuroblastoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-lb-165.

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Powers, John T., Kaloyan M. Tsanov, Frederik Roles, Richard Ebright, Marc Seligson, Yvanka de Soysa, Patrick Cahan, et al. "Abstract LB-290: Multiple distinct mechanisms disrupt let-7 miRNA biogenesis and function in neuroblastoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-290.

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Hojo, Nozomi, Alyse Huisken, Hanmin Wang, Evgeny Chirshev, Sang Nguyen, Carlotta Glackin, Yevgeniya Ioffe, and Juli Unternaehrer. "Abstract 1989: Mechanism of tumor suppressor miRNA let-7 downregulation in ovarian cancer: The epithelial-mesenchymal transition factor Snail is associated with stemness and represses let-7." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1989.

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Huisken, Alyse, Nozomi Hojo, Hanmin Wang, Evgeny Chirshev, Carlotta Glackin, Yevgeniya Ioffe, and Julia J. Unternaehrer-Hamm. "Abstract A73: Mechanism of tumor suppressor miRNA let-7 downregulation in ovarian cancer: The epithelial-mesenchymal transition factor Snail is associated with stemness and represses let-7." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a73.

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Nasreen, Najmunnisa, Nazli Khodayari, Kamal A. Mohammed, Michael Jantz, and Eugene P. Goldberg. "EphrinA1 Inhibits Tumor Growth Via Let-7 MiRNA Expression And Repression Of RAS Oncogene In Malignant Mesothelioma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5155.

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Georgiev, Todor, Krasimir Avramov, Aneliya Draganova, Valentin Dichev, Nikolay Mehterov, and Kiril Terziyski. "Downregulation of miRNA-125b and let-7 provides a novel aspect to chronic insomnia disorder – a pilot study." In ERS Sleep and Breathing 2023 abstracts. European Respiratory Society, 2023. http://dx.doi.org/10.1183/23120541.sleepandbreathing-2023.125.

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Dalay, Nejat, Zubeyde Yalniz, and Orkun Gurbuz. "Abstract A48: The K-ras let-7 miRNA binding site variant and K-ras mutations in colon cancer." In Abstracts: AACR Special Conference on RAS Oncogenes: From Biology to Therapy; February 24-27, 2014; Lake Buena Vista, FL. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.rasonc14-a48.

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Menezes, Miriam-Rose, Goeun Bae, Yong Sung Park, Julien Balzeau, Clifford C. Stephan, and John P. Hagan. "Abstract 1244: Anin vitrobiological assay to identify small molecule upregulators of let-7 miRNA in LIN28- positive ovarian cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1244.

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VIDARD, Laurent, Claire MARIET, Eric BOITIER, Véronique SIERRA, Elisabeth CAVROIS, Carlos GARCIA-ECHEVERRIA, and Hélène GOULAOUIC. "Abstract 3550: Inhibition of either LIN28A or ZCCHC11 (TUT4) provides distinct effects on the expression of the let-7 miRNA family and tumor cell proliferation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3550.

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Du, Y., and J. Lu. "Abstract P5-10-15: Genetic variants located in beta2 adrenergic receptor gene (ADRB2) and miRNA let-7 binding site alter breast cancer susceptibility: a case control analysis." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p5-10-15.

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