LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer

• DOI: 10.18632/oncotarget.11962
• Publication Date: 2016-09-11T03:55:47Z
• Authors: Whitney S. Henry; David G. Hendrickson; Francisco Beca; Benjamin Glass; Marianne Lindahl-...; Lizhi He; Zhe Ji; Kevin Struhl; Andrew H. Beck; John L. Rinn; Alex Toker
• Keywords: Ectopic expression

// Whitney S. Henry 1,* , David G. Hendrickson 2,3,* Francisco Beca 1 Benjamin Glass Marianne Lindahl-Allen 4 Lizhi He Zhe Ji Kevin Struhl Andrew H. Beck John L. Rinn 2,3 and Alex Toker Department of Pathology, Beth Israel Deaconess Medical Center, Harvard School, Boston, MA, USA 2 Stem Cell Regenerative Biology, University, Cambridge, 3 Broad Institute MIT Harvard, Biological Chemistry Molecular Pharmacology, * These authors have contributed equally to this work Correspondence to: Toker, email: Rinn, Keywords : lncRNA, Src, PI3K, breast cancer, LINC00520 Received March 29, 2016 Accepted September 02, Published 10, Abstract Long non-coding RNAs (lncRNAs) been implicated in normal cellular homeostasis as well pathophysiological conditions, including cancer. Here we performed global gene expression profiling mammary epithelial cells transformed by oncogenic v-Src identified a large subset uncharacterized lncRNAs potentially involved cancer development. Specifically, our analysis revealed novel that is upregulated upon ectopic manner dependent on the transcription factor STAT3. Similarly, also increased PI3K its decreased knockdown mutant PIK3CA. Additional highlight elevated human carcinomas, with preferential enrichment basal-like molecular subtype. ShRNA-mediated depletion results cell migration loss invasive structures 3D. RNA sequencing uncovers several genes are differentially expressed LINC00520, significant which induced -transformed MCF10A cells. Together, these findings characterize lncRNA regulated PIK3CA STAT3, may contribute etiology