Evidence map›Paper›PMID 27556690›Full record

ArticleOncotarget2016

Ataxia-telangiectasia mutated activation mediates tumor necrosis factor-alpha induced MMP-13 up-regulation and metastasis in lung cancer cells.

Hong Qiong Yan, Di Zhang, Yuan Yuan Shi, Xiang You, Lei Shi, Qing Li, Feng Guang Gao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Observational
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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

7 authors at 1 institution in 1 country.

Hong Qiong YanDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Di ZhangDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Yuan Yuan ShiDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Xiang YouDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Lei ShiDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Qing LiDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Feng Guang GaoDepartment of Immunology, Basic Medicine Science, Medical College, Xiamen University, Xiamen 361102, People's Republic of China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite that ataxia-telangiectasia mutated (ATM) is involved in IL-6 promoted lung cancer chemotherapeutic resistance and metastasis, the exact role of ATM in tumor necrosis factor-alpha (TNF-α) increasing tumor migration is still elusive. In the present study, we demonstrated that TNF-α promoted lung cancer cell migration by up-regulation of matrix metalloproteinase-13 (MMP-13). Notably, by gene silencing or kinase inhibition, we proposed for the first time that ATM is a key up-stream regulator of TNF-α activated ERK/p38-NF-κB pathway. The existence of TNF-α secreted in autocrine or paracrine manner by components of tumor microenvironment highlights the significance of TNF-α in inflammation-associated tumor metastasis. Importantly, in vivo lung cancer metastasis test showed that ATM depletion actually reduce the number of metastatic nodules and cancer nests in lung tissues, verifying the critical role of ATM in metastasis. In conclusion, our findings demonstrate that ATM, which could be activated by lung cancer-associated TNF-α, up-regulate MMP-13 expression and thereby augment tumor metastasis. Therefore, ATM might be a promising target for prevention of inflammation-associated lung cancer metastasis.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAnimalsAtaxia Telangiectasia Mutated ProteinsBone Marrow CellsCell Line, TumorCell MovementExtracellular Signal-Regulated MAP KinasesFemaleGene SilencingHumansInflammationLeukocytes, MononuclearLung NeoplasmsMatrix Metalloproteinase 13MiceAtaxia Telangiectasia Mutated ProteinsATM protein, humanExtracellular Signal-Regulated MAP KinasesMatrix Metalloproteinase 13MMP13 protein, humanNF-kappa BRNA, Small InterferingTNF protein, humanTumor Necrosis Factor-alphaataxia-telangiectasia mutatedlung cancermatrix metalloproteinasesmigrationtumor necrosis factor-alpha

Identifiers

PMID27556690
PMCPMC5308711
OpenAlexW2518608472

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.