Evidence map›Paper›PMID 27626181›Full record

ArticleOncotarget2016

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

Whitney S Henry, David G Hendrickson, Francisco Beca, Benjamin Glass, Marianne Lindahl-Allen, Lizhi He, Zhe Ji, Kevin Struhl, Andrew H Beck, John L Rinn and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 51 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Whitney S HenryDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
David G HendricksonDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
Francisco BecaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Benjamin GlassDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Marianne Lindahl-AllenDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Lizhi HeDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Zhe JiDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Kevin StruhlDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Andrew H BeckDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
John L RinnDepartment of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA, USA.
Alex TokerDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Harvard University · USBeth Israel Deaconess Medical Center · USBroad Institute · US

Funding

Genomic targets of oncoproteins and tumor suppressorsR01CA107486 · NCI · HARVARD MEDICAL SCHOOL · PI STRUHL, KEVIN · 2006 to 2020
$9.4M
INFORMATICS METHODS AND MODELS FOR COMPUTATIONAL PATHOLOGYK22LM011931 · NLM · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BECK, ANDREW H · 2014 to 2016
$476k
Identifying lincRNAs that Mediate PI 3 Kinase Dependent Breast CancerR21CA181143 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TOKER, ALEX · 2014 to 2015
$416k
NCI NIH HHS R01 CA107486NCI NIH HHS R21 CA181143NLM NIH HHS K22 LM011931
6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have been implicated in normal cellular homeostasis as well as pathophysiological conditions, including cancer. Here we performed global gene expression profiling of mammary epithelial cells transformed by oncogenic v-Src, and identified a large subset of uncharacterized lncRNAs potentially involved in breast cancer development. Specifically, our analysis revealed a novel lncRNA, LINC00520 that is upregulated upon ectopic expression of oncogenic v-Src, in a manner that is dependent on the transcription factor STAT3. Similarly, LINC00520 is also increased in mammary epithelial cells transformed by oncogenic PI3K and its expression is decreased upon knockdown of mutant PIK3CA. Additional expression profiling highlight that LINC00520 is elevated in a subset of human breast carcinomas, with preferential enrichment in the basal-like molecular subtype. ShRNA-mediated depletion of LINC00520 results in decreased cell migration and loss of invasive structures in 3D. RNA sequencing analysis uncovers several genes that are differentially expressed upon ectopic expression of LINC00520, a significant subset of which are also induced in v-Src-transformed MCF10A cells. Together, these findings characterize LINC00520 as a lncRNA that is regulated by oncogenic Src, PIK3CA and STAT3, and which may contribute to the molecular etiology of breast cancer.

Indexed as

Breast NeoplasmsCell MovementCell ProliferationCell Transformation, NeoplasticClass I Phosphatidylinositol 3-KinasesFemaleGene Expression Regulation, NeoplasticHumansMammary Glands, HumanMCF-7 CellsMutationNeoplasm InvasivenessOncogene Protein pp60(v-src)RNA InterferenceRNA, Long NoncodingSignal TransductionClass I Phosphatidylinositol 3-KinasesOncogene Protein pp60(v-src)PIK3CA protein, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription Factorbreast cancerLINC00520lncRNAPI3KSrc

Identifiers

PMID27626181
PMCPMC5347668
OpenAlexW2510173848

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.