Evidence map›Paper›PMID 25746001›Full record

ArticleOncogene2015

ECM1 regulates tumor metastasis and CSC-like property through stabilization of β-catenin.

K-m Lee, K Nam, S Oh, J Lim, R K Kim, D Shim, J-h Choi, S-J Lee, J-H Yu, J W Lee 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 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Biomarkers of tumor invasiveness in proteomics (Review).International journal of oncology · 2020
    Pooled it
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  20. The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023
    Review

3 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

K-m LeeDepartment of Life Science, Hanyang University, Seoul, Korea.
K NamDepartment of Life Science, Hanyang University, Seoul, Korea.
S OhDepartment of Life Science, Hanyang University, Seoul, Korea.
J LimDepartment of Life Science, Hanyang University, Seoul, Korea.
R K KimDepartment of Life Science, Hanyang University, Seoul, Korea.
D ShimDepartment of Life Science, Hanyang University, Seoul, Korea.
J-h ChoiDepartment of Life Science, Hanyang University, Seoul, Korea.
S-J LeeDepartment of Life Science, Hanyang University, Seoul, Korea.
J-H YuDepartment of Surgery, College of Medicine, University of Ulsan and Asan Medical Center, Seoul, Korea.
J W LeeDepartment of Surgery, College of Medicine, University of Ulsan and Asan Medical Center, Seoul, Korea.
S H AhnDepartment of Surgery, College of Medicine, University of Ulsan and Asan Medical Center, Seoul, Korea.
I ShinDepartment of Life Science, Hanyang University, Seoul, Korea.
Hanyang University · KRUniversity of Ulsan · KRAsan Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular Matrix Protein 1 (ECM1) is a marker for tumorigenesis and is correlated with invasiveness and poor prognosis in various types of cancer. However, the functional role of ECM1 in cancer metastasis is unclear. Here, we detected high ECM1 level in breast cancer patient sera that was associated with recurrence of tumor. The modulation of ECM1 expression affected not only cell migration and invasion, but also sphere-forming ability and drug resistance in breast cancer cell lines. In addition, ECM1 regulated the gene expression associated with the epithelial to mesenchymal transition (EMT) progression and cancer stem cell (CSC) maintenance. Interestingly, ECM1 increased β-catenin expression at the post-translational level through induction of MUC1, which was physically associated with β-catenin. Indeed, the association between β-catenin and the MUC1 cytoplasmic tail was increased by ECM1. Furthermore, forced expression of β-catenin altered the gene expression that potentiated EMT progression and CSC phenotype maintenance in the cells. These data provide evidence that ECM1 has an important role in cancer metastasis through β-catenin stabilization.

Indexed as

beta CateninCell Line, TumorCell MovementDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionExtracellular Matrix ProteinsFemaleHumansMucin-1Neoplasm InvasivenessNeoplasm MetastasisNeoplastic Stem CellsProtein Stabilitybeta CateninCTNNB1 protein, humanECM1 protein, humanExtracellular Matrix ProteinsMUC1 protein, humanMucin-1

Identifiers

PMID25746001
OpenAlexW2085533220

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.