Evidence map›Paper›PMID 31190277›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2020

Stromal fibroblast-derived MFAP5 promotes the invasion and migration of breast cancer cells via Notch1/slug signaling.

Z Chen, X Yan, K Li, Y Ling, H Kang

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. International journal of molecular sciences · 2025
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  4. Loss of MFAP5 and Its Effect on Skin Homeostasis and Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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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

5 authors at 1 institution in 1 country.

Z ChenDepartment of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
X YanSchool of Basic Medical Sciences, Capital Medical University, Beijing, China.
K LiDepartment of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Y LingDepartment of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
H KangDepartment of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China. drkanghua@163.com.ORCID http://orcid.org/0000-0002-1230-7961
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe tumor microenvironment (TME) regulates tumor progression, and cancer-associated fibroblasts (CAFs) are the primary stromal components of the TME, with the potential to drive tumor metastasis via the secretion of paracrine factors, but the specific mechanisms driving this process have not been defined.

methodsProteins secreted from CAFs and normal fibroblasts (NFs) were analyzed via proteomic analysis (fold change > 2, p < 0.05) to identify tumor-promoting proteins secreted by CAFs.

resultsProteomic analysis revealed that microfibrillar-associated protein 5 (MFAP5) is preferentially expressed and secreted by CAFs relative to NFs, which was confirmed by Western blotting and RT-qPCR. Transwell and wound healing assays confirmed that MFAP5 is secreted by CAFs, and drives the invasion and migration of MCF7 breast cancer cells. We further found that in MCF7 cells MFAP5 promoted epithelial-mesenchymal transition, activating Notch1 signaling and consequently upregulating NICD1 and slug. When Notch1 was knocked down in MCF7 cells, the ability of MFAP5 to promote invasion and migration decreased.

conclusionCAFs promote cancer cells invasion and migration via MFAP5 secretion and activation of the Notch1/slug signaling. These data highlight this pathway as a therapeutic target to disrupt tumor progression through the interference of CAF-tumor crosstalk.

Indexed as

Breast NeoplasmsCancer-Associated FibroblastsCell MovementContractile ProteinsEpithelial-Mesenchymal TransitionFemaleHumansIntercellular Signaling Peptides and ProteinsMCF-7 CellsNeoplasm InvasivenessReceptor, Notch1Signal TransductionSnail Family Transcription FactorsTumor MicroenvironmentContractile ProteinsIntercellular Signaling Peptides and ProteinsMFAP5 protein, humanNOTCH1 protein, humanReceptor, Notch1SNAI1 protein, humanSnail Family Transcription FactorsBreast cancerCancer-associated fibroblastsInvasionMetastasisMFAP5

Identifiers

PMID31190277
OpenAlexW2952979748

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.