Evidence map›Paper›PMID 28846832›Full record

ArticleMolecular oncology2017

Induction of a novel isoform of the lncRNA HOTAIR in Claudin-low breast cancer cells attached to extracellular matrix.

Miao Li, Xi Li, Yan Zhuang, Erik K Flemington, Zhen Lin, Bin Shan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

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  18. LncRNAInternational journal of molecular sciences · 2019
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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

6 authors at 2 institutions in 2 countries.

Miao LiDepartment of Microbiology and Parasitology, College of Basic Medical Sciences, China Medical University, Shenyang, China.
Xi LiDepartment of Biomedical Sciences, Elson S. Floyd College of Medicine, Washington State University Spokane, WA, USA.
Yan ZhuangDepartment of Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Erik K FlemingtonDepartment of Pathology, Tulane University School of Medicine, New Orleans, LA, USA.
Zhen LinDepartment of Pathology, Tulane University School of Medicine, New Orleans, LA, USA.
Bin ShanDepartment of Biomedical Sciences, Elson S. Floyd College of Medicine, Washington State University Spokane, WA, USA.
Tulane University · USWashington State University Spokane · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2012 to 2026
$69.1M
Translational Genomics Core (TGC)P20GM121288 · NIGMS · LSU HEALTH SCIENCES CENTER · PI Luis Del Valle · 2017 to 2026
$22.4M
"Project 3" MHV68 IncRNA/miRNA interaction in latency and lympomagenesisP01CA214091 · NCI · UNIVERSITY OF FLORIDA · PI ERIK K FLEMINGTON · 2017 to 2026
$15.9M
Epstein Barr virus antisense transcriptionR01AI106676 · NIAID · TULANE UNIVERSITY OF LOUISIANA · PI FLEMINGTON, ERIK K · 2014 to 2018
$1.9M
NCI NIH HHS P01 CA214091NIAID NIH HHS R01 AI106676NIGMS NIH HHS P20 GM121288NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

Elevated overexpression of the lncRNA HOTAIR mediates invasion and metastasis in breast cancer. In an apparent paradox, we observed low expression of HOTAIR in the invasive Claudin-low MDA-MB-231 and Hs578T cells in two-dimensional culture (2D). However, HOTAIR expression exhibited robust induction in laminin-rich extracellular matrix-based three-dimensional organotypic culture (lrECM 3D) over that in 2D culture. Induction of HOTAIR required intact ECM signaling, namely integrin α2 and SRC kinase activity. Moreover, invasive growth was suppressed by HOTAIR-specific siRNA. Induction of HOTAIR in lrECM 3D culture resulted from the activation of a novel isoform of HOTAIR (HOTAIR-N) whose transcription is started from the first intron of the HOXC11 gene. The HOTAIR-N promoter exhibited increased trimethylation of histone H3 lysine 4, a histone marker of active transcription, and binding of BRD4, a reader of transcriptionally active histone markers. Inhibition of BRD4 substantially reduced the expression of HOTAIR in lrECM 3D culture. In summary, our results indicate that HOTAIR expression is activated by BRD4 binding to a novel HOTAIR-N promoter in Claudin-low breast cancer cells that are attached to ECM. Induction of HOTAIR is required for invasive growth of Claudin-low breast cancer cells in lrECM 3D culture.

Indexed as

Gene Expression Regulation, NeoplasticBreast NeoplasmsBromodomain Containing ProteinsCell AdhesionCell Culture TechniquesCell Cycle ProteinsClaudinsEpigenesis, GeneticExtracellular MatrixFemaleHumansNuclear ProteinsPromoter Regions, GeneticRNA, Long NoncodingTranscription FactorsBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsClaudinsHOTAIR long untranslated RNA, humanNuclear ProteinsRNA, Long NoncodingTranscription FactorsepigeneticsHOTAIRlncRNAthree-dimensional organotypic culture

Identifiers

PMID28846832
PMCPMC5709615
OpenAlexW2748452569

What OpenQuestion holds

Textmetadata
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.