Evidence map›Paper›PMID 36140753›Full record

ReviewGenes2022

Crosstalk between Hypoxia and Extracellular Matrix in the Tumor Microenvironment in Breast Cancer.

Yasmin Dekker, Sylvia E Le Dévédec, Erik H J Danen, Qiuyu Liu

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.6field-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

41 citing papers in PubMed, 55 citations in OpenAlex.

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  12. Targeting collagen Prolyl 4-hydroxylase for cancer treatment.Medical oncology (Northwood, London, England) · 2025
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  20. Cancer stem cells in meningiomas: novel insights and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
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

4 authors at 2 institutions in 2 countries.

Yasmin DekkerLeiden Academic Centre for Drug Research, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-4511-0081
Sylvia E Le DévédecLeiden Academic Centre for Drug Research, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-0615-9616
Erik H J DanenLeiden Academic Centre for Drug Research, Leiden University, 2333 CC Leiden, The Netherlands.ORCID 0000-0002-0491-6345
Qiuyu LiuSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing 100102, China.ORCID 0000-0003-0622-266X
Leiden University · NLBeijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Even though breast cancer is the most diagnosed cancer among women, treatments are not always successful in preventing its progression. Recent studies suggest that hypoxia and the extracellular matrix (ECM) are important in altering cell metabolism and tumor metastasis. Therefore, the aim of this review is to study the crosstalk between hypoxia and the ECM and to assess their impact on breast cancer progression. The findings indicate that hypoxic signaling engages multiple mechanisms that directly contribute to ECM remodeling, ultimately increasing breast cancer aggressiveness. Second, hypoxia and the ECM cooperate to alter different aspects of cell metabolism. They mutually enhance aerobic glycolysis through upregulation of glucose transport, glycolytic enzymes, and by regulating intracellular pH. Both alter lipid and amino acid metabolism by stimulating lipid and amino acid uptake and synthesis, thereby providing the tumor with additional energy for growth and metastasis. Third, YAP/TAZ signaling is not merely regulated by the tumor microenvironment and cell metabolism, but it also regulates it primarily through its target c-Myc. Taken together, this review provides a better understanding of the crosstalk between hypoxia and the ECM in breast cancer. Additionally, it points to a role for the YAP/TAZ mechanotransduction pathway as an important link between hypoxia and the ECM in the tumor microenvironment, driving breast cancer progression.

Indexed as

Breast NeoplasmsTumor MicroenvironmentAmino AcidsExtracellular MatrixFemaleGlucoseHumansHypoxiaLipidsMechanotransduction, CellularTranscription FactorsAmino AcidsGlucoseLipidsTranscription Factorsbreast cancercell metabolismextracellular matrixhypoxiamechanotransductiontumor microenvironmentYAP/TAZ

Identifiers

PMID36140753
PMCPMC9498429
OpenAlexW4294792997

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.