Ca2+ as a therapeutic target in cancer

被引：20
作者：
Gross, Scott [1 ]
Mallu, Pranava [1 ]
Joshi, Hinal [1 ]
Schultz, Bryant [1 ]
Go, Christina [1 ]
Soboloff, Jonathan [1 ,2 ]
机构：
[1] Temple Univ, Lewis Katz Sch Med, Fels Inst Canc Res & Mol Biol, Philadelphia, PA 19122 USA
[2] Temple Univ, Lewis Katz Sch Med, Dept Med Genet & Mol Biochem, Philadelphia, PA 19122 USA
来源：
ADVANCES IN CANCER RESEARCH, VOL 148 | 2020年 / 148卷
关键词：
PROTEIN-KINASE-C; NF-KAPPA-B; ANDROGEN-DEPRIVATION THERAPY; ACTIVATED T-CELLS; EPIDERMAL-GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; RECEPTOR POTENTIAL CHANNELS; MYELOID LINEAGE COMMITMENT; CAPACITATIVE CALCIUM-ENTRY; TRANSCRIPTION FACTOR NFAT1;
D O I：
10.1016/bs.acr.2020.05.003
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Ca2+ is a ubiquitous and dynamic second messenger molecule that is induced by many factors including receptor activation, environmental factors, and voltage, leading to pleiotropic effects on cell function including changes in migration, metabolism and transcription. As such, it is not surprising that aberrant regulation of Ca2+ signals can lead to pathological phenotypes, including cancer progression. However, given the highly context-specific nature of Ca2+-dependent changes in cell function, delineation of its role in cancer has been a challenge. Herein, we discuss the distinct roles of Ca2+ signaling within and between each type of cancer, including consideration of the potential of therapeutic strategies targeting these signaling pathways.
引用
收藏
页码：233 / 317
页数：85
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