Evidence map›Paper›PMID 29467226›Full record

ArticleThe Journal of biological chemistry2018

E4BP4/NFIL3 modulates the epigenetically repressed RAS effector RASSF8 function through histone methyltransferases.

Isai Pratha Karthik, Pavitra Desai, Sudarkodi Sukumar, Aleksandra Dimitrijevic, Krishnaraj Rajalingam, Sundarasamy Mahalingam

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. A new border for circadian rhythm gene NFIL3 in diverse fields of cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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

6 authors at 2 institutions in 2 countries.

Isai Pratha KarthikFrom the Laboratory of Molecular Virology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology, Indian Institute of Technology-Madras, Chennai 600 036, India and.
Pavitra DesaiFrom the Laboratory of Molecular Virology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology, Indian Institute of Technology-Madras, Chennai 600 036, India and.
Sudarkodi SukumarFrom the Laboratory of Molecular Virology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology, Indian Institute of Technology-Madras, Chennai 600 036, India and.
Aleksandra DimitrijevicMolecular Signaling Unit-Forschungszentrum für Immuntherapie, Institute of Immunology, University Medical Center, Johannes Gutenberg-Universität, 55131 Mainz, Germany.
Krishnaraj RajalingamMolecular Signaling Unit-Forschungszentrum für Immuntherapie, Institute of Immunology, University Medical Center, Johannes Gutenberg-Universität, 55131 Mainz, Germany.
Sundarasamy MahalingamFrom the Laboratory of Molecular Virology, National Cancer Tissue Biobank, Bhupat and Jyoti Mehta School of Biosciences, Department of Biotechnology, Indian Institute of Technology-Madras, Chennai 600 036, India and mahalingam@iitm.ac.in.
Indian Institute of Technology Madras · INJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

RAS proteins are major human oncogenes, and most of the studies are focused on enzymatic RAS effectors. Recently, nonenzymatic RAS effectors (RASSF, RAS association domain family) have garnered special attention because of their tumor-suppressive properties in contrast to the oncogenic potential of the classical enzymatic RAS effectors. Whereas most members of RASSF family are deregulated by promoter hypermethylation, RASSF8 promoter remains unmethylated in many cancers but the mechanism(s) of its down-regulation remains unknown. Here, we unveil E4BP4 as a critical transcriptional modulator repressing RASSF8 expression through histone methyltransferases, G9a and SUV39H1. In line with these observations, we noticed a negative correlation of RASSF8 and E4BP4 expression in primary breast tumor samples. In addition, our data provide evidence that E4BP4 attenuates RASSF8-mediated anti-proliferation and apoptosis, shedding mechanistic insights into RASSF8 down-regulation in breast cancers. Collectively, our study provides a better understanding on the epigenetic regulation of RASSF8 function and implicates the development of better treatment strategies.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticBasic-Leucine Zipper Transcription FactorsBreast NeoplasmsFemaleHEK293 CellsHistocompatibility AntigensHistone-Lysine N-MethyltransferaseHumansMCF-7 CellsMethyltransferasesNeoplasm ProteinsRepressor ProteinsTumor Suppressor ProteinsBasic-Leucine Zipper Transcription FactorsEHMT2 protein, humanHistocompatibility AntigensHistone-Lysine N-MethyltransferaseMethyltransferasesNeoplasm ProteinsNFIL3 protein, humanRASSF8 protein, humanRepressor ProteinsSUV39H1 protein, humanTumor Suppressor Proteinsapoptosisbreast cancercell proliferationE4BP4G9ahistone methylationRas proteinRASSF8SUV39H1tumor cell biologytumor suppressor gene

Identifiers

PMID29467226
PMCPMC5900760
OpenAlexW2788562918

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.