Evidence map›Paper›PMID 23851503›Full record

ArticleOncogene2014

Autocrine/paracrine mechanism of interleukin-17B receptor promotes breast tumorigenesis through NF-κB-mediated antiapoptotic pathway.

C-K Huang, C-Y Yang, Y-M Jeng, C-L Chen, H-H Wu, Y-C Chang, C Ma, W-H Kuo, K-J Chang, J-Y Shew and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 117 citations in OpenAlex.

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  13. IL25American journal of cancer research · 2023
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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

11 authors at 3 institutions in 1 country.

C-K Huang1] Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, Taiwan [2] Genomics Research Center, Academia Sinica, Taipei, Taiwan.
C-Y YangGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Y-M JengDepartment of Pathology, National Taiwan University Hospital, Taipei, Taiwan.
C-L ChenGenomics Research Center, Academia Sinica, Taipei, Taiwan.
H-H WuGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Y-C ChangGenomics Research Center, Academia Sinica, Taipei, Taiwan.
C MaGenomics Research Center, Academia Sinica, Taipei, Taiwan.
W-H KuoDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
K-J Chang1] Department of Surgery, National Taiwan University Hospital, Taipei, Taiwan [2] Cheng Chin General Hospital, Taichung, Taiwan.
J-Y Shew1] Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, Taiwan [2] Genomics Research Center, Academia Sinica, Taipei, Taiwan.
W-H Lee1] Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, Taiwan [2] Genomics Research Center, Academia Sinica, Taipei, Taiwan [3] Department of Biological Chemistry, University of California, Irvine, CA, USA.
Genomics Research Center, Academia Sinica · TWNational Taiwan University Hospital · TWNational Taiwan University · TW

Funding

Transcriptional Role of BRCA1 in Breast CancerR01CA094170 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI LEE, WEN-HWA · 2002 to 2012
$2.7M
NCI NIH HHS CA94170
6 · The paper itself

Abstract

Gain of function of membrane receptor was a good strategy exploited by cancer cells to benefit own growth and survival. Overexpression of HER2 has been found to serve as a target for developing trastuzumab to treat 20-25% of breast cancer. However, little or none of the other membrane receptor was found to be useful as a potential target for breast cancer treatment since then. Here, we showed that amplified signaling of interleukin-17 receptor B (IL-17RB) and its ligand IL-17B promoted tumorigenicity in breast cancer cells and impeded acinus formation in immortalized normal mammary epithelial cells. External signal transmitted through IL-17RB activated nuclear factor-κB to upregulate antiapoptotic factor Bcl-2 and induced etoposide resistance. Elevated expression of IL-17RB had a stronger correlation with poor prognosis than HER2 in breast cancer patients. Interestingly, breast cancer patients with high expression of IL-17RB and HER2 had the shortest survival rate. Depletion of IL-17RB in trastuzumab-resistant breast cancer cells significantly reduced their tumorigenic activity, suggesting that IL-17RB and HER2 have an independent role in breast carcinogenesis. Furthermore, treatment with antibodies specifically against IL-17RB or IL-17B effectively attenuated tumorigenicity of breast cancer cells. These results suggest that the amplified IL-17RB/IL-17B signaling pathways may serve as a therapeutic target for developing treatment to manage IL-17RB-associated breast cancer.

Indexed as

CarcinogenesisAnimalsApoptosisAutocrine CommunicationBreast NeoplasmsCell Line, TumorErb-b2 Receptor Tyrosine KinasesEtoposideFemaleGene Expression Regulation, NeoplasticHumansInterleukin-17Mammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred NODErb-b2 Receptor Tyrosine KinasesEtoposideInterleukin-17NF-kappa BReceptors, Interleukin-17

Identifiers

PMID23851503
OpenAlexW2048785398

What OpenQuestion holds

Textmetadata
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.