Evidence map›Paper›PMID 27619757›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Targeting interleukin-1 receptor-associated kinase 1 for human hepatocellular carcinoma.

Ning Li, Jinhua Jiang, Jing Fu, Ting Yu, Bibo Wang, Wenhao Qin, An Xu, Mengchao Wu, Yao Chen, Hongyang Wang

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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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.

Ning LiState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Jinhua JiangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Jing FuInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Ting YuInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Bibo WangInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Wenhao QinInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
An XuInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Mengchao WuInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Yao ChenInternational Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute/Hospital, 225 Changhai Road, Shanghai, 200438, People's Republic of China.
Hongyang WangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China. hywangk@vip.sina.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterleukin-1 receptor associated kinase 1 (IRAK1), as a down-stream of toll-like receptor (TLR) signaling, plays important roles in series of malignancies. However, the role of IRAK1 in hepatocellular carcinoma (HCC) remains little known.

methodsIn our study, reverse transcription-PCR (RT-PCR), Western Blot, and immunohistochemical staining were used to assess the mRNA and protein levels of IRAK1 in clinical samples and cell lines. Cell counting assay and flow cytometry were employed to analyze the effect of IRAK1 on cell cycle and apoptosis. Transwell assay was used to study the role of IRAK1 in cell migration. Moreover, subcutaneous xenograft tumor models predict the efficacy of targeting IRAK1 against HCC in vivo.

resultsIRAK1 was over-expressed in HCC tissues and cell lines. Suppression of IRAK1 by small interference RNA (siRNA) or a pharmaceutical IRAK1/4 inhibitor impeded cell growth, induced apoptosis and lessened HCC xenograft tumor growth. Particularly, IRAK1/4 inhibitor treatment caused G1/S cell cycle arrest and apoptosis, confirming IRAK1 as a new therapeutic target for HCC.

conclusionIRAK1 promotes cell proliferation and protects against apoptosis in HCC, and can be a novel target for HCC treatment.

Indexed as

AnimalsApoptosisCarcinoma, HepatocellularCell CycleCell Line, TumorGene Expression Regulation, NeoplasticHep G2 CellsHumansInterleukin-1 Receptor-Associated KinasesLiver NeoplasmsMiceNeoplasm TransplantationRNA, Small InterferingUp-RegulationInterleukin-1 Receptor-Associated KinasesRNA, Small InterferingApoptosisCell cycleHepatocellular carcinomaIRAK1ProliferationSubcutaneous tumor

Identifiers

PMID27619757
PMCPMC5020546

What OpenQuestion holds

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LicenceCC BY
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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.