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The Gαh-PLCδ1 signaling axis drives metastatic progression in triple-negative breast cancer

Overview of attention for article published in Journal of Hematology & Oncology, June 2017
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Title
The Gαh-PLCδ1 signaling axis drives metastatic progression in triple-negative breast cancer
Published in
Journal of Hematology & Oncology, June 2017
DOI 10.1186/s13045-017-0481-4
Pubmed ID
Authors

Shang-Pen Huang, Pei-Yao Liu, Chih-Jung Kuo, Chi-Long Chen, Wei-Jiunn Lee, Yu-Hui Tsai, Yuan-Feng Lin

Abstract

Distant metastasis of triple-negative breast cancer (TNBC) to other organs, e.g., the lungs, has been correlated with poor survival rates among breast cancer patients. Therefore, the identification of useful therapeutic targets to prevent metastasis or even inhibit tumor growth of TNBC is urgently needed. Gαh is a novel GTP-binding protein and known as an inactive form of calcium-dependent tissue transglutaminase. However, the functional consequences of transamidating and G-protein activities of tissue transglutaminase in promoting cancer metastasis are still controversial. Kaplan-Meier analyses were performed to estimate the prognostic values of Gαh and PLCδ1 by utilizing public databases and performing immunohistochemical staining experiments. Cell-based invasion assays and in vivo lung colony-forming and orthotropic lung metastasis models were established to evaluate the effectiveness of interrupting the protein-protein interaction (PPI) between Gαh and PLCδ1 in inhibiting the invasive ability and metastatic potential of TNBC cells. Here, we showed that the increased level of cytosolic, not extracellular, Gαh is a poor prognostic marker in breast cancer patients and correlates with the metastatic evolution of TNBC cells. Moreover, clinicopathological analyses revealed that the combined signature of high Gαh/PLCδ1 levels indicates worse prognosis in patients with breast cancer and correlates with lymph node metastasis of ER-negative breast cancer. Blocking the PPI of the Gαh/PLCδ1 complex by synthetically myristoylated PLCδ1 peptide corresponding to the Gαh-binding interface appeared to significantly suppress cellular invasiveness in vitro and inhibit lung metastatic colonies of TNBC cells in vivo. This study establishes Gαh/PLCδ1 as a poor prognostic factor for patients with estrogen receptor-negative breast cancers, including TNBCs, and provides therapeutic value by targeting the PPI of the Gαh/PLCδ1 complex to combat the metastatic progression of TNBCs.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 17 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 17 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 4 24%
Student > Master 3 18%
Researcher 2 12%
Student > Doctoral Student 1 6%
Student > Ph. D. Student 1 6%
Other 1 6%
Unknown 5 29%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 18%
Medicine and Dentistry 3 18%
Agricultural and Biological Sciences 3 18%
Pharmacology, Toxicology and Pharmaceutical Science 1 6%
Chemistry 1 6%
Other 1 6%
Unknown 5 29%
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 16 January 2018.
All research outputs
#18,583,054
of 23,016,919 outputs
Outputs from Journal of Hematology & Oncology
#931
of 1,198 outputs
Outputs of similar age
#242,196
of 317,494 outputs
Outputs of similar age from Journal of Hematology & Oncology
#29
of 43 outputs
Altmetric has tracked 23,016,919 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,198 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.4. This one is in the 13th percentile – i.e., 13% 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 317,494 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 43 others from the same source and published within six weeks on either side of this one. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.