Evidence map›Paper›PMID 24632605›Full record

ArticleOncogene2015

Extracellular calumenin suppresses ERK1/2 signaling and cell migration by protecting fibulin-1 from MMP-13-mediated proteolysis.

Q Wang, B Shen, L Chen, P Zheng, H Feng, Q Hao, X Liu, L Liu, S Xu, J Chen and 1 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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

29 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Calumenin, a CaBiology · 2023
    Article
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  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
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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

11 authors at 1 institution in 1 country.

Q WangState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
B ShenState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
L ChenState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
P ZhengState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
H FengState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
Q HaoState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
X LiuState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
L LiuState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
S XuState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
J Chen1] State Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China [2] Center for Quantitative Biology, Peking University, Beijing, China.
J TengState Key Laboratory of Bio-Membrane and Membrane Bio-Engineering, Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, Department of Cell Biology and Genetics, College of Life Sciences, Peking University, Beijing, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular proteins are vital for cell activities, such as cell migration. Calumenin is highly conserved among eukaryotes, but its functions are largely unclear. Here, we identify extracellular calumenin as a suppressor of cell migration and tumor metastasis. Calumenin binds to and stabilizes fibulin-1, leading to inactivation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) signaling. We further identify the minimal functional domain of calumenin (amino acids 74-138 and 214-280). Depletion of calumenin induces fibulin-1- and phospho-ERK1/2 (pERK1/2)-dependent promotion of cell migration. Consistently, in hepatocellular and pancreatic carcinoma, both calumenin and fibulin-1 are downregulated. Furthermore, we show that matrix metalloproteinase-13 (MMP-13) proteolyzes fibulin-1 and that calumenin protects fibulin-1 from cleavage by MMP-13. Calumenin, together with fibulin-1, also interacts with fibronectin and depends on both syndecan-4 and α5β1-integrin to suppress ERK1/2 signaling and inhibit cell migration. Thus, extracellular calumenin regulates fibulin-1 to have crucial roles in ERK1/2 signaling and cell migration.

Indexed as

MAP Kinase Signaling SystemProteolysisAnimalsCalcium-Binding ProteinsCell MovementDown-RegulationExtracellular SpaceFemaleHEK293 CellsHeLa CellsHumansMatrix Metalloproteinase 13MCF-7 CellsMiceMice, Inbred C57BLMice, TransgenicCalcium-Binding ProteinsCalu protein, mousefibulinMatrix Metalloproteinase 13Mmp13 protein, mouse

Identifiers

PMID24632605
OpenAlexW2018427238

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.