Evidence map›Paper›PMID 24927102›Full record

ArticlePloS one2014

TCDD promotes lung tumors via attenuation of apoptosis through activation of the Akt and ERK1/2 signaling pathways.

Rong-Jane Chen, Shih-He Siao, Chung-Huei Hsu, Chu-Yung Chang, Louis W Chang, Chih-Hsiung Wu, Pinpin Lin, Ying-Jan Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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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

8 authors at 4 institutions in 1 country.

Rong-Jane ChenDepartment of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan; Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
Shih-He SiaoDepartment of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.
Chung-Huei HsuDepartment of Nuclear Medicine, Taipei Medical University Hospital, Taipei, Taiwan.
Chu-Yung ChangDepartment of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan.
Louis W ChangNational Environmental Health Research Center, National Health Research Institutes, Zhunan Town, Taiwan.
Chih-Hsiung WuDepartment of Surgery, School of Medicine, Taipei Medical University-Shuang Ho Hospital, Taipei, Taiwan; Center of Excellence for Cancer Research, Taipei Medical University, Taipei, Taiwan.
Pinpin LinDivision of Environmental Health and Occupational Medicine, National Health Research Institutes, Zhunan Town, Taiwan; National Environmental Health Research Center, National Health Research Institutes, Zhunan Town, Taiwan.
Ying-Jan WangDepartment of Environmental and Occupational Health, National Cheng Kung University Medical College, Tainan, Taiwan; Department of Biomedical Informatics, Asia University, Taichung, Taiwan.
National Cheng Kung University · TWNational Health Research Institutes · TWTaipei Medical University · TWTaipei Medical University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a multiple-site, multiple-species carcinogen that induces cancer in multiple organs. The molecular mechanisms underlying TCDD-induced lung tumorigenesis remain unclear. In the present study, a two-stage lung tumorigenesis model was established by administrating a single low dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) combined with TCDD to female A/J mice. The results indicated that TCDD combined with low-dose NNK has a significant tumor-promoting effect compared with TCDD or low-dose NNK alone. Resistance to apoptosis is a hallmark of cancer and is thought to be one of the tumor-promoting mechanisms regulated by TCDD. We performed an additional series of experiments in the normal human bronchial epithelial cell line Beas2B cells, in which TCDD was combined with the apoptosis inducer staurosporine. Our in vitro results confirmed that TCDD could rescue cells from apoptosis induced by staurosporine. The inhibition of apoptosis is likely mediated by the activation of the Akt and ERK1/2 pathways, as determined by the effectiveness of pathway-specific inhibitors in abrogating the anti-apoptotic activity of TCDD. In conclusion, we demonstrated that TCDD promoted NNK-induced lung tumorigenesis and revealed that TCDD inhibits staurosporine-induced apoptosis, at least in part, through the Akt and ERK1/2 signaling pathways.

Indexed as

AnimalsApoptosisCarcinogens, EnvironmentalCell LineCell ProliferationCocarcinogenesisDrug SynergismEnzyme InhibitorsFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMAP Kinase Signaling SystemMiceNitrosaminesPolychlorinated Dibenzodioxins4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanoneCarcinogens, EnvironmentalEnzyme InhibitorsNitrosaminesPolychlorinated DibenzodioxinsStaurosporine

Identifiers

PMID24927102
PMCPMC4057150
OpenAlexW1973792044

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.