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Gallic acid inhibition of Src-Stat3 signaling overcomes acquired resistance to EGF receptor tyrosine kinase inhibitors in advanced non-small cell lung cancer

Overview of attention for article published in Oncotarget, July 2016
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#46 of 9,018)
  • High Attention Score compared to outputs of the same age (97th percentile)
  • High Attention Score compared to outputs of the same age and source (98th percentile)

Mentioned by

news
12 news outlets

Citations

dimensions_citation
16 Dimensions

Readers on

mendeley
20 Mendeley
Title
Gallic acid inhibition of Src-Stat3 signaling overcomes acquired resistance to EGF receptor tyrosine kinase inhibitors in advanced non-small cell lung cancer
Published in
Oncotarget, July 2016
DOI 10.18632/oncotarget.10581
Pubmed ID
Authors

Ai N.H. Phan, Tuyen N.M. Hua, Min-Kyu Kim, Vu T.A. Vo, Jong-Whan Choi, Hyun-Won Kim, Jin Kyung Rho, Ki Woo Kim, Yangsik Jeong

Abstract

Tyrosine kinase inhibitors (TKIs) targeting epidermal growth factor receptor (EGFR) have clinically benefited to lung cancer patients harboring a subset of activating EGFR mutations. However, even with the remarkable therapeutic response at the initial TKI treatment, most lung cancer patients eventually have relapsed aggressive tumors due to acquired resistance to the TKIs. Here, we report that 3, 4, 5-trihydroxybenzoic acid or gallic acid (GA), a natural polyphenolic compound, shows anti-tumorigenic effects in TKI-resistant non-small cell lung cancer (NSCLC). Using both in vitro growth assay and in vivo xenograft animal model, we demonstrated tumor suppressive effect of GA was more selective for the TKI-resistant cancer compared to the TKI-sensitive one. Mechanistically, GA treatment inhibited Src-Stat3-mediated signaling and decreased the expression of Stat3-regulated tumor promoting genes, subsequently inducing apoptosis and cell cycle arrest in the TKI-resistant lung cancer but not in the TKI-sensitive one. Consistent with the in vitro results, in vivo xenograft experiments showed the TKI-resistant tumor-selective growth inhibition and suppression of Src-Stat3-dependent signaling in the GA-treated tumors isolated from the xenograft model. This finding identified an importance of Src-Stat3 signaling cascade in GA-mediated tumor-suppression activity and, more importantly, provides a novel therapeutic insight of GA for advanced TKI-resistant lung cancer.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 25%
Student > Bachelor 3 15%
Other 2 10%
Professor 1 5%
Student > Doctoral Student 1 5%
Other 3 15%
Unknown 5 25%
Readers by discipline Count As %
Medicine and Dentistry 5 25%
Biochemistry, Genetics and Molecular Biology 4 20%
Pharmacology, Toxicology and Pharmaceutical Science 2 10%
Agricultural and Biological Sciences 2 10%
Materials Science 1 5%
Other 0 0%
Unknown 6 30%

Attention Score in Context

This research output has an Altmetric Attention Score of 86. 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 05 October 2016.
All research outputs
#105,990
of 8,477,503 outputs
Outputs from Oncotarget
#46
of 9,018 outputs
Outputs of similar age
#7,215
of 253,458 outputs
Outputs of similar age from Oncotarget
#12
of 960 outputs
Altmetric has tracked 8,477,503 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 98th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 9,018 research outputs from this source. They receive a mean Attention Score of 3.2. This one has done particularly well, scoring higher than 99% of its peers.
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 253,458 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 97% of its contemporaries.
We're also able to compare this research output to 960 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 98% of its contemporaries.