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Golgi tethering factor golgin-97 suppresses breast cancer cell invasiveness by modulating NF-κB activity

Overview of attention for article published in Cell Communication and Signaling, April 2018
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Title
Golgi tethering factor golgin-97 suppresses breast cancer cell invasiveness by modulating NF-κB activity
Published in
Cell Communication and Signaling, April 2018
DOI 10.1186/s12964-018-0230-5
Pubmed ID
Authors

Rae-Mann Hsu, Cai-Yan Zhong, Chih-Liang Wang, Wei-Chao Liao, Chi Yang, Shih-Yu Lin, Jia-Wei Lin, Hsiao-Yun Cheng, Po-Yu Li, Chia-Jung Yu

Abstract

Golgin-97 is a tethering factor in the trans-Golgi network (TGN) and is crucial for vesicular trafficking and maintaining cell polarity. However, the significance of golgin-97 in human diseases such as cancer remains unclear. We searched for a potential role of golgin-97 in cancers using Kaplan-Meier Plotter ( http://kmplot.com ) and Oncomine ( www.oncomine.org ) datasets. Specific functions of golgin-97 in migration and invasion were examined in golgin-97-knockdown and golgin-97-overexpressing cells. cDNA microarray, pathway analysis and qPCR were used to identify gene profiles regulated by golgin-97. The role of golgin-97 in NF-κB signaling pathway was examined by using subcellular fractionation, luciferase reporter assay, western blot analysis and immunofluorescence assay (IFA). We found that low expression of golgin-97 correlated with poor overall survival of cancer patients and was associated with invasiveness in breast cancer cells. Golgin-97 knockdown promoted cell migration and invasion, whereas re-expression of golgin-97 restored the above phenotypes in breast cancer cells. Microarray and pathway analyses revealed that golgin-97 knockdown induced the expression of several invasion-promoting genes that were transcriptionally regulated by NF-κB p65. Mechanistically, golgin-97 knockdown significantly reduced IκBα protein levels and activated NF-κB, whereas neither IκBα levels nor NF-κB activity was changed in TGN46- or GCC185-knockdown cells. Conversely, golgin-97 overexpression suppressed NF-κB activity and restored the levels of IκBα in golgin-97-knockdown cells. Interestingly, the results of Golgi-disturbing agent treatment revealed that the loss of Golgi integrity was not involved in the NF-κB activation induced by golgin-97 knockdown. Moreover, both TGN-bound and cytosolic golgin-97 inhibited NF-κB activation, indicating that golgin-97 functions as an NF-κB suppressor regardless of its subcellular localization. Our results collectively demonstrate a novel and suppressive role of golgin-97 in cancer invasiveness. We also provide a new avenue for exploring the relationship between the TGN, golgin-97 and NF-κB signaling in tumor progression.

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The data shown below were collected from the profiles of 2 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 18 100%

Demographic breakdown

Readers by professional status Count As %
Student > Doctoral Student 3 17%
Student > Ph. D. Student 2 11%
Librarian 1 6%
Lecturer > Senior Lecturer 1 6%
Professor 1 6%
Other 3 17%
Unknown 7 39%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 28%
Medicine and Dentistry 3 17%
Agricultural and Biological Sciences 1 6%
Materials Science 1 6%
Engineering 1 6%
Other 0 0%
Unknown 7 39%
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 30 April 2018.
All research outputs
#17,947,156
of 23,045,021 outputs
Outputs from Cell Communication and Signaling
#638
of 1,015 outputs
Outputs of similar age
#236,901
of 326,468 outputs
Outputs of similar age from Cell Communication and Signaling
#11
of 19 outputs
Altmetric has tracked 23,045,021 research outputs across all sources so far. This one is in the 19th percentile – i.e., 19% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,015 research outputs from this source. They receive a mean Attention Score of 4.0. This one is in the 22nd percentile – i.e., 22% 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 326,468 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 22nd percentile – i.e., 22% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 19 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.