Evidence map›Paper›PMID 25069039›Full record

ArticleCancer letters2014

Critical roles for nitric oxide and ERK in the completion of prosurvival autophagy in 4OHTAM-treated estrogen receptor-positive breast cancer cells.

Lei Duan, Brian Danzer, Victor V Levenson, Carl G Maki

Abstract read
In one paragraph

Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 52 citations in OpenAlex.

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  7. Açai (Molecules (Basel, Switzerland) · 2021
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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

4 authors at 1 institution in 1 country.

Lei DuanDepartment of Anatomy and Cell Biology, Rush University Medical Center, 1750 W Harrison Street, Chicago, IL 60612, USA. Electronic address: lei_duan@rush.edu.
Brian DanzerDepartment of Radiation Oncology, Rush University Medical Center, 1750 W Harrison Street, Chicago, IL 60612, USA.
Victor V LevensonDepartment of Radiation Oncology, Rush University Medical Center, 1750 W Harrison Street, Chicago, IL 60612, USA.
Carl G MakiDepartment of Anatomy and Cell Biology, Rush University Medical Center, 1750 W Harrison Street, Chicago, IL 60612, USA. Electronic address: carl_maki@rush.edu.
Rush University Medical Center · US

Funding

Cellular Responses to p53 Activation by Nutlin-3aR01CA137598 · NCI · RUSH UNIVERSITY MEDICAL CENTER · PI MAKI, CARL G · 2009 to 2013
$1.5M
NCI NIH HHS 1R01CA137598-01A1NCI NIH HHS R01 CA137598
6 · The paper itself

Abstract

Autophagy is a mechanism of tamoxifen (TAM) resistance in ER-positive (ER+) breast cancer cells. In this study, we showed in ER+ MCF7 cells that 4-hydroxytamoxifen (4OHTAM) induced cellular nitric oxide (NO) that negatively regulates cellular superoxide (O2-) and cytotoxicity. 4OHTAM stimulated LC3 lipidation and formation of monodansylcadaverine (MDC)-labeled autophagic vesicles dependent on O2-. Depletion of NO increased O2- and LC3 lipidation, yet reduced formation of MDC-labeled autophagic vesicles. Instead, NO-depleted cells formed remarkably large vacuoles with rims decorated by LC3. The vacuoles were not labeled by MDC or the acidic lysosome-specific fluorescence dye acridine orange (AO). The vacuoles were increased by the late stage autophagy inhibitor chloroquine, which also increased LC3 lipidation. These results suggest NO is required for proper autophagic vesicle formation or maturation at a step after LC3 lipidation. In addition, 4OHTAM induced O2--dependent activation of ERK, inhibition of which destabilized lysosomes/autolysosomes upon 4OHTAM treatment and together with depletion of NO led to necrotic cell death. These results suggest an essential role for endogenous NO and ERK activation in the completion of pro-survival autophagy.

Indexed as

Antineoplastic AgentsAutophagyBreast NeoplasmsExtracellular Signal-Regulated MAP KinasesFemaleHumansMAP Kinase Signaling SystemMCF-7 CellsMicrotubule-Associated ProteinsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIIOxygenPhagosomesProtein Processing, Post-TranslationalReceptors, EstrogenafimoxifeneAntineoplastic AgentsExtracellular Signal-Regulated MAP KinasesMAP1LC3A protein, humanMicrotubule-Associated ProteinsNitric OxideNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINOS2 protein, humanNOS3 protein, humanOxygenReceptors, EstrogenTamoxifenAutophagyBreast cancerEstrogen receptorNitric oxideReactive oxygen speciesTamoxifen

Identifiers

PMID25069039
PMCPMC4827626
OpenAlexW2096378955

What OpenQuestion holds

Textmetadata
LicenceTDM
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.