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Cancer progression by breast tumors with Pit-1-overexpression is blocked by inhibition of metalloproteinase (MMP)-13

Overview of attention for article published in Breast Cancer Research, December 2014
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Title
Cancer progression by breast tumors with Pit-1-overexpression is blocked by inhibition of metalloproteinase (MMP)-13
Published in
Breast Cancer Research, December 2014
DOI 10.1186/s13058-014-0505-8
Pubmed ID
Authors

Juan Sendon-Lago, Samuel Seoane, Noemi Eiro, Maria A Bermudez, Manuel Macia, Tomas Garcia-Caballero, Francisco J Vizoso, Roman Perez-Fernandez

Abstract

IntroductionThe POU class 1 homeobox 1 transcription factor (POU1F1, also known as Pit-1) is expressed in the mammary gland and its overexpression induces profound phenotypic changes in proteins involved in cell proliferation, apoptosis, and invasion. Patients with breast cancer and elevated expression of Pit-1 show a positive correlation with the occurrence of distant metastasis. In this study we evaluate the relationship between Pit-1 and two collagenases: matrix metalloproteinase-1 (MMP-1) and matrix metalloproteinase-13 (MMP-13), which have been related to metastasis in breast cancer.MethodsWe began by transfecting the MCF-7 and MDA-MB-231 human breast adenocarcinoma cell lines with the Pit-1 overexpression vector (pRSV-hPit-1). Afterwards, the mRNA, protein, and transcriptional regulation of both MMP-1 and MMP-13 were evaluated by real-time PCR, Western blot, chromatin immuneprecipitation (ChIP), and luciferase reporter assays. We also evaluated Pit-1 overexpression with MMP-1 and MMP-13 knockdown in an severe combined immunodeficiency (SCID) mouse tumor xenograft model. Finally, by immunohistochemistry we correlated Pit-1 with MMP-1 and MMP-13 protein expression in 110 human breast tumors samples.ResultsOur data show that Pit-1 increases mRNA and protein of both MMP-1 and MMP-13 through direct transcriptional regulation. In SCID mice, knockdown of MMP-13 completely blocked lung metastasis in Pit-1 overexpressing MCF-7 cells injected into the mammary fat pad. In breast cancer patients, expression of Pit-1 was found to be positively correlated with the presence of both MMP-1 and MMP-13.ConclusionsOur data indicates that Pit-1 regulates MMP-1 and MMP-13, and that inhibition of MMP-13 blocked invasiveness to lung in Pit-1overexpressed breast cancer cells.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 31 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 29%
Student > Ph. D. Student 6 19%
Student > Master 5 16%
Student > Bachelor 3 10%
Other 2 6%
Other 1 3%
Unknown 5 16%
Readers by discipline Count As %
Agricultural and Biological Sciences 9 29%
Biochemistry, Genetics and Molecular Biology 8 26%
Medicine and Dentistry 5 16%
Computer Science 2 6%
Decision Sciences 1 3%
Other 1 3%
Unknown 5 16%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 21 December 2014.
All research outputs
#22,759,802
of 25,374,647 outputs
Outputs from Breast Cancer Research
#1,883
of 2,053 outputs
Outputs of similar age
#307,479
of 360,089 outputs
Outputs of similar age from Breast Cancer Research
#41
of 50 outputs
Altmetric has tracked 25,374,647 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,053 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 12.2. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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