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Updated: Oct 14, 2025

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CaMKK2 facilitates Golgi-associated vesicle trafficking to sustain cancer cell proliferation

Lorna M Stewart1, Lisa Gerner2, Mandy Rettel3

  • 1Patrick G Johnston Centre for Cancer Research, Queen's University Belfast, 97 Lisburn Road, Belfast, BT9 7AE, UK.

Cell Death & Disease
|November 2, 2021
PubMed

Insights

Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) impacts cell metabolism and proliferation. Knocking down CaMKK2 disrupts vesicle trafficking, leading to organelle dysfunction and impaired cell growth.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is known to regulate metabolism and support tumor growth.
  • The precise cellular mechanisms by which CaMKK2 influences cellular processes remain incompletely understood.

Purpose of the Study:

  • To investigate the subcellular consequences of altering CaMKK2 expression.
  • To elucidate the role of CaMKK2 in maintaining cellular homeostasis and proliferation.

Main Methods:

  • CaMKK2 knockdown was performed to assess cellular changes.
  • Proteomics was employed to identify interacting proteins.
  • Cellular imaging techniques were used to analyze organelle morphology and function.

Main Results:

  • CaMKK2 knockdown induced significant perturbations in endomembrane vesicle trafficking.
  • Gemin4 was identified as a direct interactor of CaMKK2 and COPI subunits.
  • CaMKK2 depletion resulted in Golgi expansion, ER stress, impaired autophagy, and reduced lysosomal acidification, mirroring COPI depletion phenotypes.

Conclusions:

  • CaMKK2 plays a critical role in maintaining organelle integrity and membrane trafficking.
  • CaMKK2 likely sustains cell proliferation through its regulation of these cellular processes.

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