Evidence map›Paper›PMID 24619412›Full record

ArticleThe Journal of biological chemistry2014

Histone deacetylase-3 mediates positive feedback relationship between anaphylaxis and tumor metastasis.

Sangkyung Eom, Youngmi Kim, Deokbum Park, Hansoo Lee, Yun Sil Lee, Jongseon Choe, Young Myeong Kim, Dooil Jeoung

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Sangkyung EomDepartments of Biochemistry, Kangwon National University, Chunchon 200-701.
Youngmi KimDepartments of Biochemistry, Kangwon National University, Chunchon 200-701.
Deokbum ParkDepartments of Biochemistry, Kangwon National University, Chunchon 200-701.
Hansoo LeeDepartments of Biological Sciences, College of Natural Sciences, Kangwon National University, Chunchon 200-701.
Yun Sil LeeCollege of Pharmacy, Ewha Womans University, Seoul 120-750, Korea.
Jongseon ChoeGraduate School of Medicine, Kangwon National University, Chunchon 200-701.
Young Myeong KimGraduate School of Medicine, Kangwon National University, Chunchon 200-701.
Dooil JeoungDepartments of Biochemistry, Kangwon National University, Chunchon 200-701. Electronic address: jeoungd@kangwon.ac.kr.
Kangwon National University · KREwha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic inflammation has been known to enhance the metastatic potential of tumor cells. The role of histone deacetylase-3 (HDAC3) in allergic skin inflammation was reported. We investigated HDAC3 involvement in the allergic inflammation-promotion of metastatic potential of tumor cells. Passive systemic anaphylaxis (PSA) induced HDAC3 expression and FcεRI signaling in BALB/c mice. PSA enhanced the tumorigenic and metastatic potential of mouse melanoma cells in HDAC3- and monocyte chemoattractant protein 1-(MCP1)-dependent manner. The PSA-mediated enhancement of metastatic potential involved the induction of HDAC3, MCP1, and CD11b (a macrophage marker) expression in the lung tumor tissues. We examined an interaction between anaphylaxis and tumor growth and metastasis at the molecular level. Conditioned medium from antigen-stimulated bone marrow-derived mouse mast cell cultures induced the expression of HDAC3, MCP1, and CCR2, a receptor for MCP1, in B16F1 mouse melanoma cells and enhanced migration and invasion potential of B16F1 cells. The conditioned medium from B16F10 cultures induced the activation of FcεRI signaling in lung mast cells in an HDAC3-dependent manner. FcεRI signaling was observed in lung tumors derived from B16F10 cells. Target scan analysis predicted HDAC3 to be as a target of miR-384, and miR-384 and HDAC3 were found to form a feedback regulatory loop. miR-384, which is decreased by PSA, negatively regulated HDAC3 expression, allergic inflammation, and the positive feedback regulatory loop between anaphylaxis and tumor metastasis. We show the miR-384/HDAC3 feedback loop to be a novel regulator of the positive feedback relationship between anaphylaxis and tumor metastasis.

Indexed as

Neoplasm MetastasisAnaphylaxisAnimalsBase SequenceBody TemperatureCell Line, TumorDNA PrimersFemaleHistone Deacetylase 3Histone DeacetylasesMast CellsMelanoma, ExperimentalMiceMice, Inbred BALB CMonocyte Chemoattractant ProteinsRatsDNA PrimersHistone Deacetylase 3Histone DeacetylasesMonocyte Chemoattractant ProteinsAllergyAnaphylaxisCell-Cell InteractionHistone DeacetylaseHistone Deacetylase-3MicroRNAMicroRNA-384Positive Feedback Regulatory LoopTumor Metastases

Identifiers

PMID24619412
PMCPMC4002117
OpenAlexW2034874717

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.