Evidence map›Paper›PMID 23934123›Full record

ArticleThe Journal of clinical investigation2013

HGF-MET signals via the MLL-ETS2 complex in hepatocellular carcinoma.

Shugaku Takeda, Han Liu, Satoru Sasagawa, Yiyu Dong, Paul A Trainor, Emily H Cheng, James J Hsieh

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. ETS2 promotes epithelial-to-mesenchymal transition in renal fibrosis by targeting JUNB transcription.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  12. Review
  13. The Function of the HGF/c-Met Axis in Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2020
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Microenvironment of liver regeneration in liver cancer.Chinese journal of integrative medicine · 2017
    Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Shugaku TakedaHuman Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
Han Liu
Satoru Sasagawa
Yiyu Dong
Paul A Trainor
Emily H Cheng
James J Hsieh
Memorial Sloan Kettering Cancer Center · USOsaka International Cancer Institute · JPStowers Institute for Medical Research · US

Funding

Integrated Analyses of Taspase 1 (MLL Cleaving Protease)R01CA119008 · NCI · WASHINGTON UNIVERSITY · PI HSIEH, JAMES J · 2006 to 2010
$1.3M
Molecular Mechanisms of Impaired DAN Damage Response in Leukemia PathogenesisR01CA138505 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI HSIEH, JAMES J · 2013 to 2015
$1.0M
Molecular Mechanisms of Impaired DAN Damage Response in Leukemia PathogenesisU01CA138505 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI HSIEH, JAMES J · 2011 to 2012
$746k
NCI NIH HHS CA119008NCI NIH HHS CA138505NCI NIH HHS R01 CA119008NCI NIH HHS R01 CA138505NCI NIH HHS U01 CA138505
6 · The paper itself

Abstract

HGF signals through its cognate receptor, MET, to orchestrate diverse biological processes, including cell proliferation, cell fate specification, organogenesis, and epithelial-mesenchymal transition. Mixed-lineage leukemia (MLL), an epigenetic regulator, plays critical roles in cell fate, stem cell, and cell cycle decisions. Here, we describe a role for MLL in the HGF-MET signaling pathway. We found a shared phenotype among Mll(-/-), Hgf(-/-), and Met(-/-) mice with common cranial nerve XII (CNXII) outgrowth and myoblast migration defects. Phenotypic analysis demonstrated that MLL was required for HGF-induced invasion and metastatic growth of hepatocellular carcinoma cell lines. HGF-MET signaling resulted in the accumulation of ETS2, which interacted with MLL to transactivate MMP1 and MMP3. ChIP assays demonstrated that activation of the HGF-MET pathway resulted in increased occupancy of the MLL-ETS2 complex on MMP1 and MMP3 promoters, where MLL trimethylated histone H3 lysine 4 (H3K4), activating transcription. Our results present an epigenetic link between MLL and the HGF-MET signaling pathway, which may suggest new strategies for therapeutic intervention.

Indexed as

AnimalsCarcinoma, HepatocellularEmbryo, MammalianEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHepatocyte Growth FactorHep G2 CellsHistone-Lysine N-MethyltransferaseHistonesHumansLiver Neoplasms, ExperimentalMaleMatrix Metalloproteinases, SecretedMethylationMiceETS2 protein, humanHepatocyte Growth FactorHistone-Lysine N-MethyltransferaseHistonesKMT2A protein, humanMatrix Metalloproteinases, SecretedMET protein, humanMyeloid-Lymphoid Leukemia ProteinProto-Oncogene Protein c-ets-2Proto-Oncogene Proteins c-met

Identifiers

PMID23934123
PMCPMC3696564
OpenAlexW2112650083

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.