Evidence map›Paper›PMID 26582220›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2015

[Effect of TRAF6 Downregulation on Malignant Biological Behavior of
Lung Cancer Cell Lines].

Gen Lin, Chuangzhong Huang, Guangjian Su, Huihua Hu, Haipeng Xu, Cheng Huang

Open access · greenAbstract readEnglish Abstract
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed, 3 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

6 authors at 2 institutions in 1 country.

Gen LinDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Chuangzhong HuangDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Guangjian SuDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Huihua HuDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Haipeng XuDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Cheng HuangDepartment of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Teaching Hospital, Fuzhou 350014, China.
Fujian Medical University · CNFujian Provincial Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectiveIt has been proven that tumor necrosis factor receptor-associated factor 6 (TRAF6) was a commonly amplified oncogene in lung cancer. However, the precise role of TRAF6 protein in lung cancer has not been extensively investigated. This study analyzed the effects of TRAF6 on the proliferation, apoptosis, cell cycle, migration, and invasion capability of lung cancer cell lines, as well as the potential molecular mechanisms involved.

methodsTo address the expression of TRAF6 in lung cancer cells, four lung cancer cell lines (A549, H1650, SPC-A-1 and Calu-3) were assayed to determine the expression of TRAF6 protein by Western blot and TRAF6 mRNA via qRT-PCR. Moreover, siRNA targeting TRAF6 was introduced into SPC-A-1 and Calu-3 cells. Nuclear factor-қB (NF-қB) DNA-binding activity, apoptosis rates, cell proliferation, cell cycle, migration, and invasion were determined by electrophoretic mobility shift assay, flow cytometry, MTS assay, flow cytometry, scratch test, and transwell chamber assay, respectively. Western blot analysis was also performed to evaluate the expression of the following proteins through K63-ubiquitination: P65, CD24 and CXCR4. Whole-genome sequencing analysis was conducted using a second-generation sequencer in SPC-A-1 cells.

resultsTRAF6 was highly up-expressed in SPC-A-1 and Calu-3 cell lines than the other two cells, which also showed K63-ubiquitinization in TRAF6. However, constitutive activation of NF-қB was observed only in SPC-A-1 lung cancer cells. Downregulation of TRAF6 suppressed the NF-κB activation, cell migration, and invasion but promoted the cell apoptosis of SPC-A-1 cells. Markedly decreased expression of CD24 and CXCR4 was observed in SPC-A-1 cells transfected by TRAF6 siRNA. Nevertheless, TRAF6 downregulation did not affect the proliferation and cell cycle of SPC-A-1 cells. Additionally, TRAF6 regulation did not affect the proliferation, apoptosis, cell cycle, migration, and invasion of Calu-3 cells. No mutations and no changes in gene copy numbers of TRAF6 were found by whole-exome sequencing of SPC-A-1 cells.

conclusionsTRAF6 may be involved in cell migration, invasion, and apoptosis of SPC-A-1 cells, possibly through regulating the NF-қB-CD24/CXCR4 pathway.
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Indexed as

ApoptosisCell Line, TumorCell MovementDown-RegulationHumansLung NeoplasmsNeoplasm InvasivenessNF-kappa BTNF Receptor-Associated Factor 6UbiquitinationNF-kappa BTNF Receptor-Associated Factor 6

Identifiers

PMID26582220
PMCPMC6000311
OpenAlexW2180119388

What OpenQuestion holds

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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.