Cancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Cancer Metabolism and Signaling Networks Program, Sanford Burnham Prebys Medical Discovery Institute, 10901 N. Torrey Pines Road, La Jolla, CA 92037, USA.
Cancer Cell. 2019 Sep 16;36(3):218-235. doi: 10.1016/j.ccell.2019.07.010. Epub 2019 Aug 29.
Atypical protein kinase C (aPKC) isozymes, PKCλ/ι and PKCζ, are now considered fundamental regulators of tumorigenesis. However, the specific separation of functions that determine their different roles in cancer is still being unraveled. Both aPKCs have pleiotropic context-dependent functions that can translate into tumor-promoter or -suppressive functions. Here, we review early and more recent literature to discuss how the different tumor types, and their microenvironments, might account for the selective signaling of each aPKC isotype. This is of clinical relevance because a better understanding of the roles of these kinases is essential for the design of new anti-cancer treatments.
非典型蛋白激酶 C（aPKC）同工酶 PKCλ/ι 和 PKCζ 现在被认为是肿瘤发生的基本调节因子。然而，决定它们在癌症中不同作用的具体功能分离仍在研究中。两种 aPKC 都具有多效性、上下文依赖性的功能，可以转化为促进肿瘤或抑制肿瘤的功能。在这里，我们回顾了早期和最近的文献，讨论了不同的肿瘤类型及其微环境如何解释每种 aPKC 同工型的选择性信号传递。这具有临床相关性，因为更好地了解这些激酶的作用对于设计新的抗癌治疗方法至关重要。
