Evidence map›Paper›PMID 22529897›Full record

ArticlePloS one2012

Dimethyl sulfoxide promotes the multiple functions of the tumor suppressor HLJ1 through activator protein-1 activation in NSCLC cells.

Chi-Chung Wang, Sheng-Yi Lin, Yi-Hua Lai, Ya-Jung Liu, Yuan-Lin Hsu, Jeremy J W Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

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  13. HLJ1 (DNAJB4) Gene Is a Novel Biomarker Candidate in Breast Cancer.Omics : a journal of integrative biology · 2017
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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 1 country.

Chi-Chung WangGraduate Institute of Basic Medicine, Fu Jen Catholic University, Taipei, Taiwan. 075006@mail.fju.edu.tw
Sheng-Yi Lin
Yi-Hua Lai
Ya-Jung Liu
Yuan-Lin Hsu
Jeremy J W Chen
Fu Jen Catholic University · TWNational Chung Hsing University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDimethyl sulfoxide (DMSO) is an amphipathic molecule that displays a diversity of antitumor activities. Previous studies have demonstrated that DMSO can modulate AP-1 activity and lead to cell cycle arrest at the G1 phase. HLJ1 is a newly identified tumor and invasion suppressor that inhibits tumorigenesis and cancer metastasis. Its transcriptional activity is regulated by the transcription factor AP-1. However, the effects of DMSO on HLJ1 are still unknown. In the present study, we investigate the antitumor effects of DMSO through HLJ1 induction and demonstrate the mechanisms involved. METHODS AND

findingsLow-HLJ1-expressing highly invasive CL1-5 lung adenocarcinoma cells were treated with various concentrations of DMSO. We found that DMSO can significantly inhibit cancer cell invasion, migration, proliferation, and colony formation capabilities through upregulation of HLJ1 in a concentration-dependent manner, whereas ethanol has no effect. In addition, the HLJ1 promoter and enhancer reporter assay revealed that DMSO transcriptionally upregulates HLJ1 expression through an AP-1 site within the HLJ1 enhancer. The AP-1 subfamily members JunD and JunB were significantly upregulated by DMSO in a concentration-dependent manner. Furthermore, pretreatment with DMSO led to a significant increase in the percentage of UV-induced apoptotic cells.

conclusionsOur results suggest that DMSO may be an important stimulator of the tumor suppressor protein HLJ1 through AP-1 activation in highly invasive lung adenocarcinoma cells. Targeted induction of HLJ1 represents a promising approach for cancer therapy, which also implied that DMSO may serve as a potential lead compound or coordinated ligand for the development of novel anticancer drugs.

Indexed as

ApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCell SurvivalDimethyl SulfoxideEnhancer Elements, GeneticGene ExpressionGene Expression Regulation, NeoplasticHSP40 Heat-Shock ProteinsHumansLung NeoplasmsTranscriptional ActivationTranscription Factor AP-1Tumor Suppressor ProteinsDimethyl SulfoxideDNAJB4 protein, humanHSP40 Heat-Shock ProteinsTranscription Factor AP-1Tumor Suppressor Proteins

Identifiers

PMID22529897
PMCPMC3328470
OpenAlexW2007217526

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Registered trials

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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.