Evidence map›Paper›PMID 25746000›Full record

ArticleOncogene2015

MKL1 potentiates lung cancer cell migration and invasion by epigenetically activating MMP9 transcription.

X Cheng, Y Yang, Z Fan, L Yu, H Bai, B Zhou, X Wu, H Xu, M Fang, A Shen and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.6field-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

35 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. mMolecular neurobiology · 2024
    Article
  3. Article
  4. Cytoskeleton remodeling mediated by circRNA-YBX1 phase separation suppresses the metastasis of liver cancer.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  5. Circulation · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Myeloid MKL1 Disseminates Cues to Promote Cardiac Hypertrophy in Mice.Frontiers in cell and developmental biology · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 4 institutions in 1 country.

X ChengKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
Y YangKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
Z FanKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
L YuKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
H BaiKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
B ZhouKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
X WuKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
H XuKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
M FangKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
A ShenDepartment of Key Laboratory of Inflammation and Molecular Targets, Medical College, Nantong University, Nantong, China.
Q ChenKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
Y XuKey Laboratory of Cardiovascular Disease and Department of Pathophysiology, Nanjing Medical University, Nanjing, China.
Nanjing Medical University · CNChina Pharmaceutical University · CNJiangsu Vocational College of Medicine · CNNantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant tumors are exemplified by excessive proliferation and aggressive migration/invasion contributing to increased mortality of cancer patients. Matrix metalloproteinase 9 (MMP9) expression is positively correlated with lung cancer malignancy. The mechanism underlying an elevated MMP9 expression is not clearly defined. We demonstrate here that the transcriptional modulator megakaryocytic leukemia 1 (MKL1) was activated by hypoxia and transforming growth factor (TGF-β), two prominent pro-malignancy factors, in cultured lung cancer cells. MKL1 levels were also increased in more invasive types of lung cancer in humans. Depletion of MKL1 in lung cancer cells attenuated migration and invasion both in vitro and in vivo. Overexpression of MKL1 potentiated the induction of MMP9 transcription by hypoxia and TGF-β, whereas MKL1 silencing diminished MMP9 expression. Of interest, MKL1 knockdown eliminated histone H3K4 methylation surrounding the MMP9 promoter. Further analyses revealed that MKL1 recruited ASH2, a component of the H3K4 methyltransferase complex, to activate MMP9 transcription. Depletion of ASH2 ameliorated cancer cell migration and invasion in an MMP9-dependent manner. Together our data indicate that MKL1 potentiates lung cancer cell migration and invasion by epigenetically activating MMP9 transcription.

Indexed as

AnimalsCell Line, TumorCell MovementDNA MethylationEpigenesis, GeneticEpigenomicsHumansLung NeoplasmsMatrix Metalloproteinase 9MethyltransferasesMiceNeoplasm InvasivenessPromoter Regions, GeneticTrans-ActivatorsTranscription, GeneticTransforming Growth Factor betaMatrix Metalloproteinase 9MethyltransferasesMMP9 protein, humanMRTFA protein, humanTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID25746000
OpenAlexW2058426459

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.