Evidence map›Paper›PMID 18825409›Full record

ArticleJournal of cancer research and clinical oncology2009

Regulation of TLR4-induced IL-6 response in bladder cancer cells by opposing actions of MAPK and PI3K signaling.

Yigang Qian, Junfang Deng, Haiyang Xie, Lei Geng, Lin Zhou, Yan Wang, Shenyong Yin, Xiaowen Feng, Shusen Zheng

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. The role of cytokines in ovarian cancer drug resistance.International journal of cancer · 2026
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  7. Knockdown of PLCε inhibits inflammatory cytokine release via STAT3 phosphorylation in human bladder cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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  17. Response of chondrocytes to shear stress: antagonistic effects of the binding partners Toll-like receptor 4 and caveolin-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011
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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

9 authors at 1 institution in 1 country.

Yigang QianDepartment of Hepatobiliary Pancreatic Surgery, Key Lab of Organ Transplantation of Zhejiang Province, Ministry of Public Health, The First Affiliated Hospital, School of Medicine, Zhejiang University, 310003, Hangzhou, China.
Junfang Deng
Haiyang Xie
Lei Geng
Lin Zhou
Yan Wang
Shenyong Yin
Xiaowen Feng
Shusen Zheng
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeToll-like receptor 4 (TLR4) was found to be aberrantly expressed in bladder cancer, inducing some genes expression and facilitating tumor progression. Recent data suggest that tumor associated Interleukin-6 (IL-6) correlates with tumor size and grade in bladder cancer. However, the molecule mechanisms of the induction of IL-6 response in bladder cancer cells are not well elucidated. In this study, we manage to find out whether TLR4 signaling is involved in the production of IL-6 by human bladder cancer cells, and the detailed molecule mechanisms by which IL-6 is up-regulated.

methodsWe selected human bladder cancer T24 cell line in the present study, and examined its expression of TLR4 and CD14 by using flow cytometry. TLR4 signaling was activated by lipopolysaccharide (LPS) and IL-6 secretion in culture supernatants was tested by using ELISA kit. The expression of p38, ERK, JNK and Akt were determined by western-blot analysis using specific antibodies.

resultsOur study demonstrated that CD14 and TLR4 were constitutively expressed in T24 cells and activation of TLR4 signaling by LPS resulted in phosphorylation of MAPK and PI3K pathways and up-regulation of IL-6 in dose- and time-dependent manner. Pretreatment of cells with SB203580 (inhibitor of p38) and PD98059 (inhibitor of ERK) attenuated LPS-induced IL-6 expression, whereas LY294002 (inhibitor of PI3K) markedly amplified the LPS-stimulated synthesis of IL-6.

conclusionsOur results demonstrate that activation of TLR4 signaling in bladder cancer cells induces tumor-associated IL-6 expression via activation of p38 and ERK, whereas activation of PI3K/Akt exerts an opposing action.

Indexed as

Cell Line, TumorExtracellular Signal-Regulated MAP KinasesGene Expression Regulation, NeoplasticHumansInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesToll-Like Receptor 4Urinary Bladder NeoplasmsExtracellular Signal-Regulated MAP KinasesInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID18825409
PMCPMC12160131
OpenAlexW2007963505

What OpenQuestion holds

Textmetadata
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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.