ArticleCell communication and signaling : CCS2018
Golgi tethering factor golgin-97 suppresses breast cancer cell invasiveness by modulating NF-κB activity.
Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Proteomics and transcriptomics reveal molecular subtypes and biomarkers of advanced cutaneous T-cell lymphoma.Frontiers in oncology · 2026Article
- The Impact of Golgi Organization on Cell Cycle and Cancer Development.Sub-cellular biochemistry · 2026Review
- The link between the trans-Golgi network and tumour progression.Molecular biology reports · 2025Review
- Trans-Golgi network tethering factors regulate TBK1 trafficking and promote the STING-IFN-I pathway.Cell discovery · 2025Article
- Noncanonical role of Golgi-associated macrophage TAZ in chronic inflammation and tumorigenesis.Science advances · 2025Article
- Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.Cell communication and signaling : CCS · 2025Article
- GCC2 promotes non-small cell lung cancer progression by maintaining Golgi apparatus integrity and stimulating EGFR signaling pathways.Scientific reports · 2024Article
- Connexin 43 mediated collective cell migration is independent of Golgi orientation.Biology open · 2023Article
- Review
- Golgi Complex: A Signaling Hub in Cancer.Cells · 2022Review
- Shedding Light on NF-κB Functions in Cellular Organelles.Frontiers in cell and developmental biology · 2022Review
- Endogenous and Exogenous Regulatory Signaling in the Secretory Pathway: Role of Golgi Signaling Molecules in Cancer.Frontiers in cell and developmental biology · 2022Review
- Heme oxygenase-1(HO-1) regulates Golgi stress and attenuates endotoxin-induced acute lung injury through hypoxia inducible factor-1α (HIF-1α)/HO-1 signaling pathway.Free radical biology & medicine · 2021Article
- Golgi-associated Rab GTPases implicated in autophagy.Cell & bioscience · 2021Review
- Alterations of Golgi Structural Proteins and Glycosylation Defects in Cancer.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundGolgin-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.
methodsWe 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).
resultsWe 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.
conclusionOur 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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