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STAT3 and HIF1α cooperatively activate HIF1 target genes in MDA-MB-231 and RCC4 cells

Overview of attention for article published in Oncogene, April 2013
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1 X user
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1 peer review site

Citations

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184 Mendeley
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1 CiteULike
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Title
STAT3 and HIF1α cooperatively activate HIF1 target genes in MDA-MB-231 and RCC4 cells
Published in
Oncogene, April 2013
DOI 10.1038/onc.2013.115
Pubmed ID
Authors

M R Pawlus, L Wang, C-J Hu

Abstract

Solid tumors often exhibit simultaneously inflammatory and hypoxic microenvironments. The 'signal transducer and activator of transcription-3' (STAT3)-mediated inflammatory response and the hypoxia-inducible factor (HIF)-mediated hypoxia response have been independently shown to promote tumorigenesis through the activation of HIF or STAT3 target genes and to be indicative of a poor prognosis in a variety of tumors. We report here for the first time that STAT3 is involved in the HIF1, but not HIF2-mediated hypoxic transcriptional response. We show that inhibiting STAT3 activity in MDA-MB-231 and RCC4 cells by a STAT3 inhibitor or STAT3 small interfering RNA significantly reduces the levels of HIF1, but not HIF2 target genes in spite of normal levels of hypoxia-inducible transcription factor 1α (HIF1α) and HIF2α protein. Mechanistically, STAT3 activates HIF1 target genes by binding to HIF1 target gene promoters, interacting with HIF1α protein and recruiting coactivators CREB binding protein (CBP) and p300, and RNA polymerase II (Pol II) to form enhanceosome complexes that contain HIF1α, STAT3, CBP, p300 and RNA Pol II on HIF1 target gene promoters. Functionally, the effect of STAT3 knockdown on proliferation, motility and clonogenic survival of tumor cells in vitro is phenocopied by HIF1α knockdown in hypoxic cells, whereas STAT3 knockdown in normoxic cells also reduces cell proliferation, motility and clonogenic survival. This indicates that STAT3 works with HIF1 to activate HIF1 target genes and to drive HIF1-depedent tumorigenesis under hypoxic conditions, but also has HIF-independent activity in normoxic and hypoxic cells. Identifying the role of STAT3 in the hypoxia response provides further data supporting the effectiveness of STAT3 inhibitors in solid tumor treatment owing to their usefulness in inhibiting both the STAT3 and HIF1 pro-tumorigenic signaling pathways in some cancer types.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 184 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 4 2%
United Kingdom 4 2%
Korea, Republic of 1 <1%
Malaysia 1 <1%
Czechia 1 <1%
Unknown 173 94%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 61 33%
Researcher 28 15%
Student > Master 19 10%
Student > Bachelor 14 8%
Professor 8 4%
Other 27 15%
Unknown 27 15%
Readers by discipline Count As %
Agricultural and Biological Sciences 51 28%
Biochemistry, Genetics and Molecular Biology 48 26%
Medicine and Dentistry 22 12%
Immunology and Microbiology 7 4%
Pharmacology, Toxicology and Pharmaceutical Science 5 3%
Other 13 7%
Unknown 38 21%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 19 October 2015.
All research outputs
#14,168,910
of 22,708,120 outputs
Outputs from Oncogene
#8,526
of 10,632 outputs
Outputs of similar age
#111,856
of 196,447 outputs
Outputs of similar age from Oncogene
#50
of 87 outputs
Altmetric has tracked 22,708,120 research outputs across all sources so far. This one is in the 35th percentile – i.e., 35% of other outputs scored the same or lower than it.
So far Altmetric has tracked 10,632 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.0. This one is in the 18th percentile – i.e., 18% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 196,447 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 87 others from the same source and published within six weeks on either side of this one. This one is in the 41st percentile – i.e., 41% of its contemporaries scored the same or lower than it.