Suppression of TRPM7 enhances TRAIL-induced apoptosis in triple-negative breast cancer cells.
Antineoplastic Agents
/ pharmacology
Apoptosis
/ genetics
Breast Neoplasms
/ drug therapy
Cell Line, Tumor
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Female
Hepatic Stellate Cells
/ drug effects
Humans
Protein Kinase Inhibitors
/ pharmacology
Protein Serine-Threonine Kinases
/ antagonists & inhibitors
TRPM Cation Channels
/ antagonists & inhibitors
Triple Negative Breast Neoplasms
/ drug therapy
TRAIL
TRPM7
apoptosis
c-FLIP
triple-negative breast cancer
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
received:
04
10
2019
revised:
03
05
2020
accepted:
15
05
2020
pubmed:
30
5
2020
medline:
7
4
2021
entrez:
30
5
2020
Statut:
ppublish
Résumé
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 Gd
Substances chimiques
Antineoplastic Agents
0
Protein Kinase Inhibitors
0
TRPM Cation Channels
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
TRPM7 protein, human
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
10037-10050Informations de copyright
© 2020 Wiley Periodicals LLC.
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