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Zhe Wang, Ke Ma, Steffie Pitts, Yulan Cheng, Xi Liu, Xiquan Ke, Samuel Kovaka, Hassan Ashktorab, Duane T Smoot, Michael Schatz, Zhirong Wang, and Stephen J Meltzer

functional assays using interference and overexpression of circNF1 revealed that circNF1 promotes cell proliferation. Finally, circNF1 functioned as a miR-16 sponge, derepressing the miR-16 target genes MAP7 and AKT3 . We conclude that circNF1

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Darrell Green, Irina Mohorianu, Iain McNamara, Tamas Dalmay, and William D Fraser

variability in the number of reads assigned to either miRNAs or tRNA fragments in the control samples (when compared to inbred genetic models such as mice and fruit flies where variability is minimal). We identified a low expression of miR-16 in PDB compared

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Goswin Y Meyer-Rochow, Nicole E Jackson, John V Conaglen, Denis E Whittle, Muthusamy Kunnimalaiyaan, Herbert Chen, Gunnar Westin, Johanna Sandgren, Peter Stålberg, Elham Khanafshar, Daniel Shibru, Quan-Yang Duh, Orlo H Clark, Electron Kebebew, Anthony J Gill, Rory Clifton-Bligh, Bruce G Robinson, Diana E Benn, and Stan B Sidhu

cancer came from the observation that the most common deletions in human chronic lymphocytic leukaemia (CLL) occur in the 13q14 chromosomal region ( Calin et al . 2002 ). Two miRNAs (miR-15 and miR-16) are located in this region and have been found to be

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Andrea Vecchione and Carlo M Croce

Caspase-3 miR-15a 13q14 Regulates pancreatic regeneration BCL-2 miR-16-1 13q14 Negatively regulates cell cycle progression and cell growth BCL-2 Regulates pancreatic regeneration miR-21 17q23 Unknown PTEN TMP1 PDCD

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Valeria Coppola, Ruggero De Maria, and Désirée Bonci

↑ ↓ ↓ miR-125b ↓ ↓ ↓ ↑ miR-128 ↓ ↓ miR-141 ↑ ↑ miR-143 ↓ ↓ miR-145 ↓ ↓ miR-146 ↑ ↓ miR-148 ↑ ↓ miR-16 ↑ ↓ ↓ ↓ miR-181

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Libero Santarpia, Milena Nicoloso, and George A Calin

cancer cell lines), miR-21 , miR-27 ( MDA-MB-231 cells), miR-29b-2 , miR-146 , miR-155 , miR-181 family, miR-373 and miR-520c (in metastatic tumors) Prostate cancers Let-7 family, miR-15a/miR-16-1 cluster, miR-101 , miR-125a

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E Patterson, R Webb, A Weisbrod, B Bian, M He, L Zhang, A K Holloway, R Krishna, N Nilubol, K Pacak, and E Kebebew

miR-16 were underexpressed in malignant as compared to benign pheochromocytomas ( Meyer-Rochow et al . 2010 ). In this study, we further evaluated the miRNA expression changes that accompany malignancy in an independent, large pheochromocytoma tumor

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Neetu Dahiya and Patrice J Morin

& Lai 2008 ). A possible link between miRs and cancer was first reported in chronic lymphocytic leukemia, where miR-15 and miR-16 were found to be deleted or down-regulated in the vast majority of tumors ( Calin et al . 2002 ). Since then, a large

Open access

Bethany Smith, Priyanka Agarwal, and Neil A Bhowmick

promoter regions. In further cross-talk within the EMT regulators, Snail1 assists in the transcriptional repression of miR-200f, to enhance EMT ( Diaz-Lopez et al. 2015 ). Importantly, miR-16 and miR-200 family members silences TGF-β signaling and blocks

Free access

Luke A Selth, Matthew J Roberts, Clement W K Chow, Villis R Marshall, Suhail A R Doi, Andrew D Vincent, Lisa M Butler, Martin F Lavin, Wayne D Tilley, and Robert A Gardiner

artefact of the lower total miRNA read count in this group. The geometric mean of three small RNAs – miR-16 , U6 and RNU48 (SNORD48) – that were stably expressed in the clinical samples (data not shown) was used for normalisation purposes. miRNAs