Evidence map›Paper›PMID 22016393›Full record

ArticleThe Journal of biological chemistry2011

Hyaluronan synthase 2 (HAS2) promotes breast cancer cell invasion by suppression of tissue metalloproteinase inhibitor 1 (TIMP-1).

Berit Bernert, Helena Porsch, Paraskevi Heldin

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
4.4field-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

65 citing papers in PubMed, 132 citations in OpenAlex.

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  11. Hyaluronic Acid as a Modern Approach in Anticancer Therapy-Review.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Article
  14. Metabolomics and EMT Markers of Breast Cancer: A Crosstalk and Future Perspective.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

5 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

3 authors at 3 institutions in 2 countries.

Berit BernertLudwig Institute for Cancer Research, Biomedical Center, Uppsala University, SE-75124 Uppsala, Sweden.
Helena PorschLudwig Institute for Cancer Research, Biomedical Center, Uppsala University, SE-75124 Uppsala, Sweden.
Paraskevi HeldinLudwig Institute for Cancer Research, Biomedical Center, Uppsala University, SE-75124 Uppsala, Sweden. Electronic address: evi.heldin@licr.uu.se.
Ludwig Cancer Research · SELudwig Cancer Research · BEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invasion and metastasis are the primary causes of breast cancer mortality, and increased knowledge about the molecular mechanisms involved in these processes is highly desirable. High levels of hyaluronan in breast tumors have been correlated with poor patient survival. The involvement of hyaluronan in the early invasive phase of a clone of breast cancer cell line MDA-MB-231 that forms bone metastases was studied using an in vivo-like basement membrane model. The metastatic to bone tumor cells exhibited a 7-fold higher hyaluronan-synthesizing capacity compared with MDA-MB-231 cells predominately due to an increased expression of hyaluronan synthase 2 (HAS2). We found that knockdown of HAS2 completely suppressed the invasive capability of these cells by the induction of tissue metalloproteinase inhibitor 1 (TIMP-1) and dephosphorylation of focal adhesion kinase. HAS2 knockdown-mediated inhibition of basement membrane remodeling was rescued by HAS2 overexpression, transfection with TIMP-1 siRNA, or addition of TIMP-1-blocking antibodies. Moreover, knockdown of HAS2 suppressed the EGF-mediated induction of the focal adhesion kinase/PI3K/Akt signaling pathway. Thus, this study provides new insights into a possible mechanism whereby HAS2 enhances breast cancer invasion.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticApoptosisBreast NeoplasmsCell Line, TumorFemaleGlucuronosyltransferaseGlycosyltransferasesHumansHyaluronan SynthasesNeoplasm InvasivenessNeoplasm MetastasisPhosphorylationRNA, Small InterferingSignal TransductionTissue Inhibitor of Metalloproteinase-1GlucuronosyltransferaseGlycosyltransferasesHAS2 protein, humanHyaluronan SynthasesRNA, Small InterferingTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID22016393
PMCPMC3234988
OpenAlexW2072228040

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.