Evidence map›Paper›PMID 27073433›Full record

ArticleExperimental and therapeutic medicine2016

IKKβ/NFκBp65 activated by interleukin-13 targets the autophagy-related genes LC3B and beclin 1 in fibroblasts co-cultured with breast cancer cells.

Wen-Lin Li, Li-Xia Xiong, Xiao-Yu Shi, Liang Xiao, Guan-Yun Qi, Chuang Meng

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  6. The effects and the mechanisms of autophagy on the cancer-associated fibroblasts in cancer.Journal of experimental & clinical cancer research : CR · 2019
    Review
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  13. IL-13 receptor α2 stimulates human glioma cell growth and metastasis through the Src/PI3K/Akt/mTOR signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  14. 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

6 authors at 2 institutions in 1 country.

Wen-Lin LiKey Laboratory of Medical Biology, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Li-Xia XiongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xiao-Yu ShiKey Laboratory of Medical Biology, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Liang XiaoMolecular Laboratory, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330006, P.R. China.
Guan-Yun QiKey Laboratory of Medical Biology, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Chuang MengKey Laboratory of Medical Biology, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Nanchang University · CNJiangxi University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-13 (IL-13), a Th2 cytokine, plays an important role in fibrosis, inflammation, tissue hyperresponsiveness and tumor development. Although studies have demonstrated that IL-13 exerts its roles through signal transducer and activator of transcription 6 (STAT6) signaling pathway, recent studies have revealed that I kappa B kinase (IKK)/nuclear factor kappa B (NFκB) pathway may also be involved in. The aim of this study was to investigate whether IL-13 delivers signals to IKKβ/NFκBp65 and whether autophagy genes are IL-13-induced the activation of NFκBp65 transcriptional targets in fibroblasts of breast tumor stroma. We examined the phosphorylation of IKKβ, the activation of NFκBp65 and NFκBp65-targeted autophagy genes in fibroblasts co-cultured with breast cancer cells under the condition of IL-13 stimulation. Results of this study showed that IL-13 induced IKKβ phosphorylation in the fibroblast line ESF co-cultured with breast cancer cell line BT474, and subsequently NFκBp65 was activated and aimed at beclin 1 and microtubule-associated protein 1 light chain 3 B (MAP1LC3B or LC3B) in these ESF cells. BMS345541, an inhibitor of IKK/NFκB pathway, significantly inhibited the IL-13-induced the activation of NFκB and also inhibited NFκB-targeted beclin 1 and LC3B expression. Our results suggest that IL-13 regulates beclin 1 and LC3B expression through IKKβ/NFκBp65 in fibroblasts co-cultured with breast cancer cells, and IL-13 plays role in activating IKKβ/NFκBp65.

Indexed as

beclin 1breast cancerfibroblastinhibitor of κB kinase βinterleukin-13microtubule-associated protein 1 light chain 3 βnuclear factor κB

Identifiers

PMID27073433
PMCPMC4812107
OpenAlexW2257603010

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.