Systemic Ablation of Camkk2 Impairs Metastatic Colonization and Improves Insulin Sensitivity in TRAMP Mice: Evidence for Cancer Cell-Extrinsic CAMKK2 Functions in Prostate Cancer

Authors

Thomas L Pulliam
Dominik Awad
Jenny J Han
Mollianne M Murray
Jeffrey J Ackroyd
Pavithr Goli
Jonathan S Oakhill
John W Scott
Michael M Ittmann
Daniel E Frigo

Language

English

Publication Date

6-10-2022

Journal

Cells

DOI

10.3390/cells11121890

PMID

35741020

PMCID

PMC9221545

PubMedCentral® Posted Date

6-10-2022

PubMedCentral® Full Text Version

Post-print

Abstract

Despite early studies linking calcium-calmodulin protein kinase kinase 2 (CAMKK2) to prostate cancer cell migration and invasion, the role of CAMKK2 in metastasis in vivo remains unclear. Moreover, while CAMKK2 is known to regulate systemic metabolism, whether CAMKK2's effects on whole-body metabolism would impact prostate cancer progression and/or related comorbidities is not known. Here, we demonstrate that germline ablation of

Keywords

Adenocarcinoma, Animals, Calcium-Calmodulin-Dependent Protein Kinase Kinase, Carcinogenesis, Cell Transformation, Neoplastic, Disease Models, Animal, Humans, Insulin Resistance, Lung Neoplasms, Male, Mice, Mice, Transgenic, Prostatic Neoplasms, Protein Kinases

Published Open-Access

yes

Recommended Citation

Pulliam, Thomas L; Awad, Dominik; Han, Jenny J; et al., "Systemic Ablation of Camkk2 Impairs Metastatic Colonization and Improves Insulin Sensitivity in TRAMP Mice: Evidence for Cancer Cell-Extrinsic CAMKK2 Functions in Prostate Cancer" (2022). Faculty and Staff Publications. 2905.
https://digitalcommons.library.tmc.edu/baylor_docs/2905