Evidence map›Paper›PMID 28211615›Full record

ArticleCancer medicine2017

Targeting of crosstalk between tumor and tumor microenvironment by β-D mannuronic acid (M2000) in murine breast cancer model.

Fatemeh Hosseini, Hadi Hassannia, Ahmad Mahdian-Shakib, Farhad Jadidi-Niaragh, Seyed Ehsan Enderami, Mohammadjavad Fattahi, Ali Anissian, Abbas Mirshafiey, Parviz Kokhaei

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 42 citations in OpenAlex.

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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

9 authors at 7 institutions in 2 countries.

Fatemeh HosseiniCancer Research Center and Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran.
Hadi HassanniaDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Ahmad Mahdian-ShakibDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Farhad Jadidi-NiaraghDrug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Seyed Ehsan EnderamiDepartment of Molecular Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Mohammadjavad FattahiDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Ali AnissianDepartment of Veterinary Medicine, Islamic Azad University, Abhar, Abhar branch, Iran.
Abbas MirshafieyDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Parviz KokhaeiCancer Research Center and Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran.ORCID 0000-0001-6544-4209
Tehran University of Medical Sciences · IRIslamic Azad University, Abhar Branch · IRKarolinska Institutet · SESemnan University of Medical Sciences · IRShiraz University of Medical Sciences · IRTabriz University of Medical Sciences · IRZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is the main cause of death in breast cancer patients. Inflammatory processes following crosstalk between tumor cells and tumor microenvironment play an important role in progression and metastasis of cancer. Hence, targeting of these interactions may represent a novel promising strategy for breast cancer therapy. So, we investigated the effects of β-D mannuronic acid (BDM), a new antiinflammatory agent, on 4T1 breast cancer cell line both in vitro and in vivo. Proliferation assays revealed low-cytotoxic effect of BDM on 4T1 cells. However, BDM reduced activity of MMP-2, MMP-9 and significantly decreased the adhesion of 4T1 cells to extracellular matrix (ECM) in a dose-dependent manner. The in vivo results demonstrated that BDM strongly inhibits tumor growth and increases lifespan as compared with control mice. The decrease in tumor mass was associated with decreased metastasis, recruitment, and frequency of inflammatory cells in tumor tissue. Our preclinical findings demonstrated that BDM therapy not only prevents formation of chronic inflammatory response but also inhibits crosstalk between tumor cells and their microenvironment, which is associated with reduction of tumor growth and metastasis arrest. Our data imply the use of BDM therapy in future clinical trials to open a new horizon for breast cancer therapy.

Indexed as

AnimalsAnti-Inflammatory AgentsBreast NeoplasmsCell AdhesionCell Line, TumorCell ProliferationDose-Response Relationship, DrugFemaleHexuronic AcidsMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceNeoplasm MetastasisTumor BurdenTumor MicroenvironmentXenograft Model Antitumor AssaysAnti-Inflammatory AgentsHexuronic Acidsmannuronic acidMatrix Metalloproteinase 2Matrix Metalloproteinase 9MMP2 protein, humanMMP9 protein, humanbreast cancerM2000metastasisβ-D-mannuronic acid

Identifiers

PMID28211615
PMCPMC5345625
OpenAlexW2587819799

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Registered trials

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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.