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RBM5-AS1 Is Critical for Self-Renewal of Colon Cancer Stem-like Cells
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2016 (Engelska)Ingår i: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 76, nr 19, s. 5615-5627Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Cancer-initiating cells (CIC) undergo asymmetric growth patterns that increase phenotypic diversity and drive selection for chemotherapeutic resistance and tumor relapse. WNT signaling is a hallmark of colon CIC, often caused by APC mutations, which enable activation of β-catenin and MYC Accumulating evidence indicates that long noncoding RNAs (lncRNA) contribute to the stem-like character of colon cancer cells. In this study, we report enrichment of the lncRNA RBM5-AS1/LUST during sphere formation of colon CIC. Its silencing impaired WNT signaling, whereas its overexpression enforced WNT signaling, cell growth, and survival in serum-free media. RBM5-AS1 has been little characterized previously, and we determined it to be a nuclear-retained transcript that selectively interacted with β-catenin. Mechanistic investigations showed that silencing or overexpression of RBM5-AS1 caused a respective loss or retention of β-catenin from TCF4 complexes bound to the WNT target genes SGK1, YAP1, and MYC Our work suggests that RBM5-AS1 activity is critical for the functional enablement of colon cancer stem-like cells. Furthermore, it defines the mechanism of action of RBM5-AS1 in the WNT pathway via physical interactions with β-catenin, helping organize transcriptional complexes that sustain colon CIC function. 

Ort, förlag, år, upplaga, sidor
2016. Vol. 76, nr 19, s. 5615-5627
Nationell ämneskategori
Cell- och molekylärbiologi
Identifikatorer
URN: urn:nbn:se:umu:diva-129272DOI: 10.1158/0008-5472.CAN-15-1824ISI: 000385625500008PubMedID: 27520449OAI: oai:DiVA.org:umu-129272DiVA, id: diva2:1058978
Tillgänglig från: 2016-12-22 Skapad: 2016-12-22 Senast uppdaterad: 2018-11-27Bibliografiskt granskad

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Aguiló, Francesca

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