Protein kinase Cλ/ι in cancer: a contextual balance of time and signals

被引：5

作者：

Moscat, Jorge ^{[1
,2
]}

Linares, Juan F. ^{[1
,2
]}

Duran, Angeles ^{[1
,2
]}

Diaz-Meco, Maria T. ^{[1
,2
]}

机构：

[1] Weill Cornell Med, Dept Pathol, 1300 York Ave, New York, NY 10065 USA

[2] Weill Cornell Med, Lab Med, 1300 York Ave, New York, NY 10065 USA

来源：

TRENDS IN CELL BIOLOGY | 2022年 / 32卷 / 12期

基金：

美国国家卫生研究院;

关键词：

NEUROENDOCRINE PHENOTYPE; INCREASED SURVIVAL; ZETA REPRESSES; PANETH CELLS; RAG GTPASES; PKC-ZETA; PROSTATE; TUMORIGENESIS; INFLAMMATION; PHOSPHORYLATION;

D O I：

10.1016/j.tcb.2022.04.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Nononcogenic cancer drivers often impinge on complex signals that create new addictions and vulnerabilities. Protein kinase CI,/iota PKCI,/iota suppresses tumorigen-esis by blocking metabolic pathways that regulate fuel oxidation and create building blocks for the epigenetic control of cell differentiation. Reduced levels of PKCI,/iota unleash these pathways to promote tumorigenesis, but the simulta-neous activation of the STING-driven interferon cascade prevents tumor initia-tion by triggering immunosurveillance mechanisms. However, depending on the context of other signaling pathways, such as WNT/beta-catenin or PKC zeta, and timing, PKCI,/iota deletion can promote or inhibit tumorigenesis. In this review, we discuss in detail the molecular and cellular underpinnings of PKCI,/iota functions in cancer with the perspective of the crosstalk between metabolism and inflam-mation in the tumor microenvironment.

引用

页码：1023 / 1034

页数：12

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