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Suppression of TRPM7 enhances TRAIL-induced apoptosis in triple-negative breast cancer cells

Authors
 Chiman Song  ;  Seunghye Choi  ;  Ki-Bong Oh  ;  Taebo Sim 
Citation
 JOURNAL OF CELLULAR PHYSIOLOGY, Vol.235(12) : 10037-10050, 2020-05 
Journal Title
 JOURNAL OF CELLULAR PHYSIOLOGY 
ISSN
 0021-9541 
Issue Date
2020-05
Keywords
TRAIL ; TRPM7 ; apoptosis ; c-FLIP ; triple-negative breast cancer
Abstract
Transient receptor potential cation channel subfamily M member 7 (TRPM7) composed of an ion channel and a kinase domain regulates triple-negative breast cancer (TNBC) cell migration, invasion, and metastasis, but it does not modulate TNBC proliferation. However, previous studies have shown that the combination treatment of nonselective TRPM7 channel inhibitors (2-aminoethoxydiphenyl borate and Gd3+ ) with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) increases antiproliferative effects and apoptosis in prostate cancer cells and hepatic stellate cells. We, therefore, investigated the potential role of TRPM7 in proliferation and apoptosis of TNBC cells (MDA-MB-231 and MDA-MB-468 cells) with TRAIL. We demonstrated that suppression of TRPM7 via TRPM7 knockdown or pharmacological inhibition synergistically increases TRAIL-induced antiproliferative effects and apoptosis in TNBC cells. Furthermore, we showed that the synergistic interaction might be associated with TRPM7 channel activities using combination treatments of TRAIL and TRPM7 inhibitors (NS8593 as a TRPM7 channel inhibitor and TG100-115 as a TRPM7 kinase inhibitor). We reveal that downregulation of cellular FLICE-inhibitory protein via inhibition of Ca2+ influx might be involved in the synergistic interaction. Our study would provide both a new role of TRPM7 in TNBC cell apoptosis and a potential combinatorial therapeutic strategy using TRPM7 inhibitors with TRAIL in the treatment of TNBC.
Full Text
https://onlinelibrary.wiley.com/doi/10.1002/jcp.29820
DOI
10.1002/jcp.29820
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Sim, Taebo(심태보)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/180320
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