Evidence map›Paper›PMID 26146406›Full record

ArticleScientific reports2015

N-Myc and STAT Interactor regulates autophagy and chemosensitivity in breast cancer cells.

Brandon J Metge, Aparna Mitra, Dongquan Chen, Lalita A Shevde, Rajeev S Samant

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

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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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

5 authors at 2 institutions in 1 country.

Brandon J MetgeDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.
Aparna MitraMitchell Cancer Institute, University of South Alabama, Mobile, AL, USA.
Dongquan Chen1] Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA [2] Comprehensive Cancer Centre, University of Alabama at Birmingham, Birmingham, AL, USA [3] Division of Preventive Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.
Lalita A Shevde1] Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA [2] Comprehensive Cancer Centre, University of Alabama at Birmingham, Birmingham, AL, USA.
Rajeev S Samant1] Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA [2] Comprehensive Cancer Centre, University of Alabama at Birmingham, Birmingham, AL, USA.
University of Alabama at Birmingham · USUSA Mitchell Cancer Institute · US

Funding

XRAY CRYSTALLOGRAPHYP30CA013148 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Robert S Welner · 1985 to 2026
$165.9M
Molecular determinants of breast cancer malignancyR01CA138850 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SHEVDE, LALITA A. · 2011 to 2015
$1.6M
Role of Nmi in retarding breast tumor growth.R01CA140472 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SAMANT, RAJEEV S · 2010 to 2014
$1.3M
NCI NIH HHS CA138850NCI NIH HHS CA140472NCI NIH HHS P30 CA013148NCI NIH HHS R01 CA138850NCI NIH HHS R01 CA140472
6 · The paper itself

Abstract

We have previously reported that expression of NMI (N-myc and STAT interactor) is compromised in invasive breast cancers. We also demonstrated that loss of NMI expression promotes epithelial-mesenchymal-transition and results in enhanced invasive ability of breast cancer cells. Additionally we had demonstrated that restoration of NMI expression reduced breast cancer xenograft growth and downregulated Wnt and TGFβ/SMAD signaling. Here we present our observations that NMI expression drives autophagy. Our studies were promoted by our observation that NMI expressing breast cancer cells showed autophagic vacuoles and LC3 processing. Additionally, we found that NMI expression increased the cisplatin sensitivity of the breast cancer cells. Our mechanistic investigations show that NMI prompts activation of GSK3-β. This multifunctional kinase is an upstream effector of the TSC1/TSC2 complex that regulates mTOR signaling. Inhibition of GSK3-β activity in NMI expressing cells activated mTOR signaling and decreased the cells' autophagic response. Additionally we demonstrate that a key component of autophagy, DNA-damage regulated autophagy modulator 1 (DRAM1), is regulated by NMI. Our TCGA database analysis reveals concurrent expression of NMI and DRAM1 in breast cancer specimens. We present evidence that NMI sensitizes breast cancer cells to cisplatin treatment through DRAM1 dependent autophagy.

Indexed as

AutophagyDrug Resistance, NeoplasmAnimalsAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCisplatinDoxorubicinFemaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, NudeAntineoplastic AgentsCisplatinDoxorubicinDRAM1 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIntracellular Signaling Peptides and ProteinsMAP1LC3A protein, humanMembrane ProteinsMicrotubule-Associated ProteinsNMI protein, humanRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID26146406
PMCPMC4648342
OpenAlexW913223666

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.