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1. IGF2BP3 Modulates the Interaction of Invasion-Associated Transcripts with RISC.

Author

Ennajdaoui H, Howard JM, Sterne-Weiler T, Jahanbani F, Coyne DJ, Uren PJ, Dargyte M, Katzman S, Draper JM, Wallace A, Cazarez O, Burns SC, Qiao M, Hinck L, Smith AD, Toloue MM, Blencowe BJ, Penalva LO, and Sanford JR

Subjects
Adenocarcinoma genetics, Adenocarcinoma pathology, Argonaute Proteins genetics, Argonaute Proteins metabolism, Carcinoma, Pancreatic Ductal genetics, Carcinoma, Pancreatic Ductal pathology, Cell Line, Tumor, Focal Adhesions metabolism, Gene Expression Regulation, Neoplastic, HeLa Cells, Humans, MicroRNAs genetics, MicroRNAs metabolism, Neoplasm Invasiveness, Polymorphism, Single Nucleotide genetics, RNA, Messenger genetics, RNA, Messenger metabolism, RNA, Neoplasm metabolism, RNA-Binding Proteins genetics, RNA-Binding Proteins metabolism, RNA-Induced Silencing Complex metabolism
Abstract

Insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) expression correlates with malignancy, but its role(s) in pathogenesis remains enigmatic. We interrogated the IGF2BP3-RNA interaction network in pancreatic ductal adenocarcinoma (PDAC) cells. Using a combination of genome-wide approaches, we have identified 164 direct mRNA targets of IGF2BP3. These transcripts encode proteins enriched for functions such as cell migration, proliferation, and adhesion. Loss of IGF2BP3 reduced PDAC cell invasiveness and remodeled focal adhesion junctions. Individual nucleotide resolution crosslinking immunoprecipitation (iCLIP) revealed significant overlap of IGF2BP3 and microRNA (miRNA) binding sites. IGF2BP3 promotes association of the RNA-induced silencing complex (RISC) with specific transcripts. Our results show that IGF2BP3 influences a malignancy-associated RNA regulon by modulating miRNA-mRNA interactions., (Copyright © 2016 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2016
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2. Mammary Stem Cell Self-Renewal Is Regulated by Slit2/Robo1 Signaling through SNAI1 and mINSC.

Author

Ballard MS, Zhu A, Iwai N, Stensrud M, Mapps A, Postiglione MP, Knoblich JA, and Hinck L

Subjects
Animals, Asymmetric Cell Division, Cell Cycle Proteins genetics, Cell Line, Tumor, Humans, Intercellular Signaling Peptides and Proteins genetics, Mammary Glands, Human growth & development, Mice, Mice, Inbred C57BL, Nerve Tissue Proteins genetics, Receptors, Immunologic genetics, Signal Transduction, Snail Family Transcription Factors, Stem Cells cytology, Stem Cells physiology, Transcription Factors genetics, Roundabout Proteins, Cell Cycle Proteins metabolism, Cell Self Renewal, Intercellular Signaling Peptides and Proteins metabolism, Mammary Glands, Human cytology, Nerve Tissue Proteins metabolism, Receptors, Immunologic metabolism, Stem Cells metabolism, Transcription Factors metabolism
Abstract

Tissue homeostasis requires somatic stem cell maintenance; however, mechanisms regulating this process during organogenesis are not well understood. Here, we identify asymmetrically renewing basal and luminal stem cells in the mammary end bud. We demonstrate that SLIT2/ROBO1 signaling regulates the choice between self-renewing asymmetric cell divisions (ACDs) and expansive symmetric cell divisions (SCDs) by governing Inscuteable (mInsc), a key member of the spindle orientation machinery, through the transcription factor Snail (SNAI1). Loss of SLIT2/ROBO1 signaling increases SNAI1 in the nucleus. Overexpression of SNAI1 increases mInsc expression, an effect that is inhibited by SLIT2 treatment. Increased mInsc does not change cell proliferation in the mammary gland (MG) but instead causes more basal cap cells to divide via SCD, at the expense of ACD, leading to more stem cells and larger outgrowths. Together, our studies provide insight into how the number of mammary stem cells is regulated by the extracellular cue SLIT2., (Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2015
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