Evidence map›Paper›PMID 26476534›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

TAB3 overexpression promotes cell proliferation in non-small cell lung cancer and mediates chemoresistance to CDDP in A549 cells via the NF-κB pathway.

Jie Chen, Jun Gu, Jian Feng, Yifei Liu, Qun Xue, Tingting Ni, Zhiwen Wang, Liangliang Jia, Guoxin Mao, Lili Ji

Abstract read
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In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. LncRNA PCIR Is an Oncogenic DriverFrontiers in oncology · 2021
    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

10 authors at 3 institutions in 1 country.

Jie ChenJiangsu Province Key Laboratory for Inflammation and Molecular Target, Medical College, Nantong University, Nantong, 226001, Jiangsu, China.
Jun GuDepartment of Respiratory, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Jian FengDepartment of Oncology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Yifei LiuDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Qun XueDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Tingting NiDepartment of Oncology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Zhiwen WangDepartment of Thoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
Liangliang JiaDepartment of Respiratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210000, Jiangsu, China.
Guoxin MaoDepartment of Oncology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China. maoguoxinnt@126.com.
Lili JiJiangsu Province Key Laboratory for Inflammation and Molecular Target, Medical College, Nantong University, Nantong, 226001, Jiangsu, China. liliji79@126.com.
Affiliated Hospital of Nantong University · CNNantong University · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-activated kinase 1 (TAK1)-binding protein 3 (TAB3) is essential for the activation of the nuclear factor kappa B (NF-κB) pathway and has important roles in cell survival. However, the contribution of TAB3 to non-small cell lung cancer (NSCLC) remains elusive. In the present study, Western blotting and immunohistochemistry assays demonstrated that TAB3 expression was frequently increased in NSCLC tissues and cells. In addition, chi-square test and Kaplan-Meier analysis revealed that upregulation of TAB3 expression correlated with a more invasive tumor phenotype and poor prognosis. In addition, a series of experiments, including serum starvation-refeeding experiment and TAB3-siRNA transfection assay, showed that TAB3 expression promoted NSCLC cell proliferation. Furthermore, the effect of TAB3 expression on the sensitivity to cis-diamminedichloroplatinum (CDDP) and possible signaling transduction pathways was investigated. When the expression of TAB3 was inhibited by siRNA transfection, the sensitivity to CDDP was enhanced. Moreover, it showed that downregulation of TAB3 enhanced CDDP-induced A549 cell apoptosis through the inhibition of the NF-κB pathway. These results suggest that TAB3 plays a critical role in NSCLC progression and chemoresistance and that TAB3 depletion may be a promising approach to lung cancer therapy.

Indexed as

A549 CellsAdaptor Proteins, Signal TransducingBlotting, WesternCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCisplatinDrug Resistance, NeoplasmFemaleHumansImmunohistochemistryIntracellular Signaling Peptides and ProteinsKaplan-Meier EstimateLung NeoplasmsMaleMiddle AgedAdaptor Proteins, Signal TransducingCisplatinIntracellular Signaling Peptides and ProteinsNF-kappa BTAB3 protein, humanChemoresistanceNF-κB pathwayNon-small cell lung cancerProliferationTAB3

Identifiers

PMID26476534
OpenAlexW2121959322

What OpenQuestion holds

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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.