Evidence map›Paper›PMID 23055197›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2013

Effect of TRAF6 on the biological behavior of human lung adenocarcinoma cell.

Lou Zhong, Fei Cao, Qingsheng You

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2013. 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
1.2field-weighted citation impact, top 20% 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, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The relationship between TRAF6 and tumors.Cancer cell international · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. [Effect of TRAF6 Downregulation on Malignant Biological Behavior of
Lung Cancer Cell Lines].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015
    Article
  11. TRAF6 is required for BLyS-mediated NF-κB signaling in multiple myeloma cells.Medical oncology (Northwood, London, England) · 2015
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. TRAF molecules in cell signaling and in human diseases.Journal of molecular signaling · 2013
    Article
  17. Article
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

3 authors at 2 institutions in 1 country.

Lou ZhongDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, 20 Xishi Road, Nantong, 226001, Jiangsu Province, People's Republic of China.
Fei Cao
Qingsheng You
Affiliated Hospital of Nantong University · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a unique adaptor protein of the tumor necrosis factor receptor-associated factor family that mediates both tumor necrosis factor receptor and interleukin-1 receptor/Toll-like receptor signaling. A recent study showed that TRAF6 played an important role in tumorigenesis and invasion through activation of nuclear factor kappa B (NF-κB). However, the biological role of TRAF6 remains unknown in lung cancer up to now. To address the expression of TRAF6 in lung cancer cells, four lung cancer cell lines (A549, HCC827, NCI-H292, and 95-D) and human bronchial epithelial cells were used to detect the expression of TRAF6 protein by western blotting. Results indicated that TRAF6 displayed an upregulation in human lung cancer cell lines. To investigate the effects of TRAF6 on the biological behavior of human lung adenocarcinoma cell, we generated human lung adenocarcinoma A549 cell line in which TRAF6 was depleted. The results showed that downregulation of TRAF6 could decrease cell viability, suppress cell proliferation and invasion, and promote cell apoptosis. At the same time, we explored the effects of TRAF6 on the expression of the following proteins: phosphor-NF-κB (p-p65), cyclin D1, caspase-3, and matrix metalloproteinase 9 (MMP9). Downregulation of TRAF6 could decrease the expression of p-p65, cyclin D1, and MMP9 and increase the expression of caspase-3. All these results suggested that TRAF6 might be involved in the potentiation of growth, proliferation, and invasion of A549 cell line, as well as the inhibition of A549 cell apoptosis by the activation of NF-κB. To make a long story short, the overexpression of TRAF6 might be related to the tumorigenesis and invasion of lung cancer.

Indexed as

AdenocarcinomaApoptosisCaspase 3Cell Line, TumorCell ProliferationCell SurvivalCell Transformation, NeoplasticCyclin D1Down-RegulationHumansLung NeoplasmsMatrix Metalloproteinase 9Neoplasm InvasivenessNF-kappa BSignal TransductionTNF Receptor-Associated Factor 6Caspase 3Cyclin D1Matrix Metalloproteinase 9NF-kappa BTNF Receptor-Associated Factor 6Transcription Factor RelA

Identifiers

PMID23055197
OpenAlexW2026647332

What OpenQuestion holds

Textmetadata
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.