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Cells
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The Roles of CaMKK2 in Cell Metabolism and Disease 2022
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The Roles of CaMKK2 in Cell Metabolism and Disease 2022

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 3009

Special Issue Editors

Prof. Dr. Jon Oakhill

E-Mail Website
Guest Editor
1. St. Vincent's Institute of Medical Research, School of Medicine, University of Melbourne, Melbourne, VIC 3052, Australia
2. Exercise and Nutrition Research Program, Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, VIC 3000, Australia
Interests: metabolism; protein structure; kinase; proteomics; cancer; diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. John W. Scott

E-Mail Website
Guest Editor
1. St. Vincent's Institute of Medical Research, Fitzroy, Melbourne, VIC 3065, Australia
2. Exercise and Nutrition Research Program, Mary MacKillop Institute for Health Research, Australian Catholic University, Melbourne, VIC 3000, Australia
3. The Florey Institute of Neuroscience and Mental Health, Parkville, VIC 3052, Australia
Interests: metabolism; kinase regulation; cell signaling; metabolic; neuropsychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The calcium-sensing enzyme Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) functions as a molecular hub to regulate critical cell functions and physiological responses. CaMKK2’s well-characterised substrates CaMK1, CaMK4, and the metabolic co-ordinator AMP-activated protein kinase (AMPK) implicate CaMKK2 signalling cascades in diverse processes including energy homeostasis, autophagy, cell survival, cell cycle, cytoskeletal remodelling, inflammation, gene expression, mRNA splicing, neuronal excitability, cognition and synaptic plasticity associated with learning and memory. CaMKK2 also directly activates the important oncogenic target AKT (PKB), underpinning recent efforts to develop small-molecule CaMKK2 inhibitors as anti-cancer drugs. In this Special Issue entitled The Roles of CaMKK2 in Cell Metabolism and Disease, we aim to capture the scope of ongoing research being conducted on CaMKK2 at the molecular, cellular and physiological levels. We are particularly interested in submissions investigating how CaMKK2 dysregulation leads to a wide range of pathologies (e.g., cancer, diabetes, osteoporosis) and psychiatric disorders. Our goal is to amalgamate recent advances in this exciting and emerging field, and to provide a platform for united commentary on the current state of play regarding the therapeutic potential of CaMKK2.

We look forward to your contributions.

Prof. Dr. Jon Oakhill
Dr. John W. Scott
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolism
  • cancer
  • appetite regulation
  • signalling
  • phosphorylation
  • calcium-calmodulin
  • kinase inhibitors

Published Papers (1 paper)

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Research

19 pages, 4884 KiB  
Article
Systemic Ablation of Camkk2 Impairs Metastatic Colonization and Improves Insulin Sensitivity in TRAMP Mice: Evidence for Cancer Cell-Extrinsic CAMKK2 Functions in Prostate Cancer
by 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 and Daniel E. Frigo
Cells 2022, 11(12), 1890; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11121890 - 10 Jun 2022
Cited by 6 | Viewed by 2574
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 [...] Read more.
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 Camkk2 slows, but does not stop, primary prostate tumorigenesis in the TRansgenic Adenocarcinoma Mouse Prostate (TRAMP) genetic mouse model. Consistent with prior epidemiological reports supporting a link between obesity and prostate cancer aggressiveness, TRAMP mice fed a high-fat diet exhibited a pronounced increase in the colonization of lung metastases. We demonstrated that this effect on the metastatic spread was dependent on CAMKK2. Notably, diet-induced lung metastases exhibited a highly aggressive neuroendocrine phenotype. Concurrently, Camkk2 deletion improved insulin sensitivity in the same mice. Histological analyses revealed that cancer cells were smaller in the TRAMP;Camkk2−/− mice compared to TRAMP;Camkk2+/+ controls. Given the differences in circulating insulin levels, a known regulator of cell growth, we hypothesized that systemic CAMKK2 could promote prostate cancer cell growth and disease progression in part through cancer cell-extrinsic mechanisms. Accordingly, host deletion of Camkk2 impaired the growth of syngeneic murine prostate tumors in vivo, confirming nonautonomous roles for CAMKK2 in prostate cancer. Cancer cell size and mTOR signaling was diminished in tumors propagated in Camkk2-null mice. Together, these data indicate that, in addition to cancer cell-intrinsic roles, CAMKK2 mediates prostate cancer progression via tumor-extrinsic mechanisms. Further, we propose that CAMKK2 inhibition may also help combat common metabolic comorbidities in men with advanced prostate cancer. Full article
(This article belongs to the Special Issue The Roles of CaMKK2 in Cell Metabolism and Disease 2022)
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