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Our study demonstrates the downregulation of micro RNA-183 (mi R-183) in retinoblastoma ( RB) tissues and RB cell lines compared with normal retinal tissues. The ectopic expression of mi R-183 in the RB cell lines Y79, SO- RB50 and WERI- RB1 suppresses cell viability, migration and invasion. Furthermore, the Wnt co-receptor low-density lipoprotein receptor-related protein 6 ( LRP6) was identified as a new target of mi R-183, and restoration of the expression of LRP6 rescues the effects induced by mi R-183 in RB cells. These results indicate that miR-183 targets and downregulates LRP6 in the growth, migration and invasion of RB cells. [ABSTRACT FROM AUTHOR]

Highlights: [•] MiR-365b-3p is downregulated in human retinoblastoma tissues. [•] MiR-365b-3p inhibits the expression of PAX6 by directly binding its 3′UTR. [•] MiR-365b-3p attenuates cell growth, induces G1 phase arrest and cell apoptosis. [•] MiR-365b-3p upregulates p21 and p27 but downregulates cdc2 and Cyclin D1 levels. [ABSTRACT FROM AUTHOR]

Retinoblastoma (RB) is an intraocular malignancy that mainly affects young children. Previous reports have demonstrated that mutations or the inactivation of the RB1 gene were the main cause of RB; however, disruption of the intracellular signaling pathways following deficiency of RB1 requires further investigation. Based on the Gene Expression Omnibus data and bioinformatics prediction, the present study aimed to investigate the microRNA (miR)-338-3p/neuro-oncological ventral antigen 1 (NOVA1) axis in RB. Subsequently, overexpression and knockdown of miR-338-3p and NOVA1, respectively, were performed to study the role of miR-338-3p/NOVA1 in the progression of the RB cells. The results demonstrated that overexpression of miR-338-3p significantly inhibited cell proliferation, migration and invasion, and promoted apoptosis of the RB cells. Moreover, knockdown of NOVA1 showed similar results. A dual-luciferase reporter assay and rescue experiments further confirmed the direct binding between miR-338-3p and NOVA1. Taken together, the results indicated that miR-338-3p acted as tumor suppressor by targeting the oncogene of NOVA1 in RB, which may serve as potential therapeutic targets in RB. [ABSTRACT FROM AUTHOR]

• In Pinus massoniana sRNA libraries, 53 conserved MicroRNAs and 41 novel MicroRNAs were identified. • With 1966 transcripts, 2606 miRNA-target pairs were predicted. • MicroRNA regulatory network and key modules involved in strobilus development were identified. Pinus massoniana (P.massoniana) is a gymnosperm with important economic value. Strobilus is an important organ for the study of morphogenesis and pattern-building mechanisms at the reproductive stage of conifers. miRNA induced post-transcriptional regulation plays a key role in sex differentiation, strobilus development, fertilization and embryogenesis in gymnosperms. In this study, miRNA profiles of strobili (female and male) and vegetative tissues of P. massoniana were constructed and compared by sRNA-seq. By de novo prediction and manual revision, 53 conserved miRNAs and 41 novel miRNAs were identified, including 30 differentially expressed miRNAs. Comprehensive analysis with computational prediction and degradome data provided 349 genes targeted by 102 miRNAs. The target gene enrichment analysis indicated that signal transduction was significantly activated during strobilus (especially male strobilus) development. The miRNA-target network was constructed and its module miRNA (miR156, 529, 396 and Nov23)- SPLs (SQUAMOSA PROMOTER BINDING PROTEIN-LIKE) seemed to be a key regulator in the differentiation of male strobili from female strobili and vegetative tissues. In addition, the precursor and primary transcripts identified with miRNA quantification indicated that the regulatory mechanism of miRNA abundance is complex and needs to be studied further. This study provides important miRNA and target information for the strobilus of P. massoniana. The de novo prediction method was appropriate for miRNA identification in plants without a reference genome. The significantly activated pathways and miRNA-target networks identified here increase the understanding of the posttranscriptional regulatory mechanism of strobilus differentiation and development in the reproductive phase of conifers. [ABSTRACT FROM AUTHOR]

The halophyte tamarisk (Tamarix) is extremely salt tolerant, making it an ideal material for salt tolerance-related studies. Although many salt-responsive genes of Tamarix were identified in previous studies, there are no reports on the role of post-transcriptional regulation in its salt tolerance. We constructed six small RNA libraries of Tamarix chinensis roots with NaCl treatments. High-throughput sequencing of the six libraries was performed and microRNA expression profiles were constructed. We investigated salt-responsive microRNAs to uncover the microRNA-mediated genes regulation. From these analyses, 251 conserved and 18 novel microRNA were identified from all small RNAs. From 191 differentially expressed microRNAs, 74 co-expressed microRNAs were identified as salt-responsive candidate microRNAs. The most enriched GO (gene ontology) terms for the 157 genes targeted by differentially expressed microRNAs suggested that transcriptions factors were highly active. Two hub microRNAs (miR414, miR5658), which connected by several target genes into an organic microRNA regulatory network, appeared to be the key regulators of post-transcriptional salt-stress responses. As the first survey on the tamarisk small RNAome, this study improves the understanding of tamarisk salt-tolerance mechanisms and will contribute to the molecular-assisted resistance breeding. [ABSTRACT FROM AUTHOR]

The pathogenesis of ischemic diseases remains unclear. Here we demonstrate the induction of microRNA-668 (miR-668) in ischemic acute kidney injury (AKI) in human patients, mice, and renal tubular cells. The induction was HIF-1 dependent, as HIF-1 deficiency in cells and kidney proximal tubules attenuated miR-668 expression. We further identified a functional HIF-1 binding site in the miR-668 gene promoter. Anti-miR-668 increased apoptosis in renal tubular cells and enhanced ischemic AKI in mice, whereas miR-668 mimic was protective. Mechanistically, anti-miR-668 induced mitochondrial fragmentation, whereas miR-668 blocked mitochondrial fragmentation during hypoxia. We analyzed miR-668 target genes through immunoprecipitation of microRNA-induced silencing complexes followed by RNA deep sequencing and identified 124 protein-coding genes as likely targets of miR-668. Among these genes, only mitochondrial protein 18 kDa (MTP18) has been implicated in mitochondrial dynamics. In renal cells and mouse kidneys, miR-668 mimic suppressed MTP18, whereas anti-miR-668 increased MTP18 expression. Luciferase microRNA target reporter assay further verified MTP18 as a direct target of miR-668. In renal tubular cells, knockdown of MTP18 suppressed mitochondrial fragmentation and apoptosis. Together, the results suggest that miR-668 is induced via HIF-1 in ischemic AKI and that, upon induction, miR-668 represses MTP18 to preserve mitochondrial dynamics for renal tubular cell survival and kidney protection. [ABSTRACT FROM AUTHOR]