Title | The Dual Roles of the Atypical Protein Kinase Cs in Cancer. |
Publication Type | Journal Article |
Year of Publication | 2019 |
Authors | Reina-Campos M, Diaz-Meco MT, Moscat J |
Journal | Cancer Cell |
Volume | 36 |
Issue | 3 |
Pagination | 218-235 |
Date Published | 2019 09 16 |
ISSN | 1878-3686 |
Keywords | Animals, Antineoplastic Agents, Cell Polarity, Cell Transformation, Neoplastic, Disease Models, Animal, Epithelial Cells, Gene Expression Regulation, Neoplastic, Humans, Isoenzymes, Mice, Transgenic, Mutation, Neoplasms, Protein Kinase C, Protein Kinase Inhibitors, Proto-Oncogenes, Signal Transduction, Tumor Microenvironment, Tumor Suppressor Proteins |
Abstract | 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. |
DOI | 10.1016/j.ccell.2019.07.010 |
Alternate Journal | Cancer Cell |
PubMed ID | 31474570 |
PubMed Central ID | PMC6751000 |
Grant List | R01 DK108743 / DK / NIDDK NIH HHS / United States R01 CA211794 / CA / NCI NIH HHS / United States R01 CA207177 / CA / NCI NIH HHS / United States R01 CA192642 / CA / NCI NIH HHS / United States R01 CA218254 / CA / NCI NIH HHS / United States |
Related Faculty:
Maria Diaz-Meco Conde, Ph.D.