Evidence map›Paper›PMID 30467308›Full record

ArticleOncogenesis2018

Upregulation of Ets1 expression by NFATc2 and NFKB1/RELA promotes breast cancer cell invasiveness.

Gi-Cheon Kim, Ho-Keun Kwon, Choong-Gu Lee, Ravi Verma, Dipayan Rudra, Taemook Kim, Keunsoo Kang, Jong Hee Nam, Young Kim, Sin-Hyeog Im

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 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

10 authors at 5 institutions in 2 countries.

Gi-Cheon KimDivision of Integrative Biosciences and Biotechnology (IBB), Department of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Ho-Keun KwonDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, 02115, USA.
Choong-Gu LeeDivision of Integrative Biosciences and Biotechnology (IBB), Department of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.ORCID http://orcid.org/0000-0002-7977-0408
Ravi VermaDivision of Integrative Biosciences and Biotechnology (IBB), Department of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.ORCID http://orcid.org/0000-0003-1859-5973
Dipayan RudraDivision of Integrative Biosciences and Biotechnology (IBB), Department of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea.
Taemook KimDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea.
Keunsoo KangDepartment of Microbiology, College of Natural Sciences, Dankook University, Cheonan, 31116, Republic of Korea.
Jong Hee NamChonnam National University Medical School, Gwangju, 501-749, Korea.
Young KimDepartment of Oral Pathology, School of Dentistry, Chonnam National University, Gwangju, 501-749, Korea.
Sin-Hyeog ImDivision of Integrative Biosciences and Biotechnology (IBB), Department of Life Sciences, Pohang University of Science and Technology, Pohang, 37673, Republic of Korea. iimsh@postech.ac.kr.ORCID http://orcid.org/0000-0002-3173-1856
Pohang University of Science and Technology · KRChonnam National University · KRDankook University · KRHarvard University · USKorea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is highly aggressive and is the leading cause of cancer-related mortality in women in developed countries. The ETS proto-oncogene 1 (Ets1) has versatile roles during the cellular processes of cancer development. It is often highly expressed in breast cancers and mediates migration and invasion of human breast cancer cells. However, underlying mechanisms of Ets1 gene expression is still ambiguous. Here, we identified a core-regulatory element (CRE) located in the Ets1 promoter region (-540/-80 bp from TSS) that contains elements responsible for associating with NFATs and NF-κBs. Compared with the less metastatic breast cancer cells, metastatic breast cancer cells (MDA-MB-231) show open chromatin configurations in the CRE, which facilitates direct binding of NFATc2 and/or NFKB1/RELA complex to trans-activate Ets1 transcription. Moreover, enhanced level of Nfatc2 and Nfkb1 positively correlated with Ets1 expression in the human breast cancer specimens. Deletion of the CRE region by CRISPR/Cas9 system resulted in significant reduction in Ets1 expression, which led to alterations of Ets1-mediated transcription programs including tumor invasiveness-related genes. Proper regulation of Ets1 gene expression by targeting the NFATc2 and NFKB1/RELA interaction could be a potential therapeutic target for Ets1-mediated metastatic breast cancer.

Identifiers

PMID30467308
PMCPMC6250664
OpenAlexW2901815786

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Registered trials

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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.