期刊
REDOX BIOLOGY
卷 28, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.redox.2019.101361
关键词
Calcium; Cell invasion; TMBIM; Golgi apparatus; Hydrogen peroxide; Metabolism
资金
- Fundacao para a Ciencia e a Tecnologia [UID/DTP/04567/2019]
- Isaac Newton grant
- STSM grant from EU-ROS COST action [BM1203]
- STSM grant from EuroCellNet COST action [CA15214]
- [UID/DTP/04567/2016]
- MRC [G0900224] Funding Source: UKRI
- Fundação para a Ciência e a Tecnologia [UID/DTP/04567/2019] Funding Source: FCT
The mechanisms by which the Golgi apparatus (GA) impacts on cell invasion are poorly understood. The human Golgi Anti-Apoptotic Protein (hGAAP, also known as TMBIM4) is a highly conserved Golgi cation channel that modulates intracellular Ca2+ fluxes. Human GAAP is expressed in all human tissues, is essential for cell viability and provides resistance against a range of apoptotic stresses. Furthermore, hGAAP enhances adhesion and cell migration by increasing the turnover of focal adhesions due to activation of store-operated Ca2+ entry. Here, we describe a GA-derived mechanism that controls cell invasion. The overexpression of hGAAP stimulates 3-dimensional proteolytic cell invasion by a mechanism that is dependent on the accumulation of intracellular hydrogen peroxide, which might be produced by the hGAAP-dependent stimulation of mitochondrial respiration. These findings provide new insight into the complex mechanisms by which Ca2+ and reactive oxygen species signaling contribute to cell invasion and to the role of the GA in these processes.
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