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The many faces of calmodulin in cell proliferation, programmed cell death, autophagy, and cancer

Martin W Berchtold1, Antonio Villalobo2

  • 1Department of Biology, University of Copenhagen, Copenhagen Biocenter 4-2-09 Ole Maaløes Vej 5, DK-2200 Copenhagen N, Denmark.

Biochimica Et Biophysica Acta
|November 6, 2013
PubMed

Insights

Calmodulin (CaM) regulates vital cell functions like proliferation and death. Targeting CaM signaling offers potential cancer therapies by impacting tumor growth and spread.

Area of Science:

  • Molecular Biology
  • Cellular Signaling
  • Cancer Research

Background:

  • Calmodulin (CaM) is a crucial calcium-binding protein found in all eukaryotic cells.
  • CaM acts as a central regulator for numerous cellular processes through interactions with diverse target proteins.

Purpose of the Study:

  • To review the role of CaM and CaM-dependent signaling in vertebrate cell proliferation, programmed cell death, and autophagy.
  • To highlight the importance of CaM in cancer cell physiology, including tumor stem cells and progression.
  • To discuss the therapeutic potential of targeting CaM-dependent pathways.

Main Methods:

  • Literature review focusing on CaM's function in cellular processes.
  • Analysis of CaM's involvement in cancer cell physiology and tumor progression.
  • Exploration of CaM-targeted therapeutic strategies.

Main Results:

  • CaM significantly influences cell proliferation, programmed cell death, and autophagy in vertebrates.
  • CaM and associated signaling pathways are critical for cancer cell physiology, tumor stem cells, angiogenesis, and metastasis.
  • CaM-dependent signaling represents a promising target for cancer therapeutics.

Conclusions:

  • Calmodulin is a key regulator of fundamental cellular processes and plays a significant role in cancer.
  • Targeting CaM-mediated signaling pathways holds potential for novel cancer treatment strategies.
  • Further research into CaM's role in cancer progression and therapeutic targeting is warranted.
Keywords:
(4-[3,5-bis-[2-(4-hydroxy-3-methoxy-phenyl)-ethyl]-4,5-dihydro-pyrazol-1-yl]-benzoic acid(4-[3,5-bis-[2-(4-hydroxy-3-methoxy-phenyl)-vinyl]-4,5-dihydro-pyrazol-1-yl]-phenyl)-(4-methyl-piperazin-1-yl)-methanone(−) enantiomer of dihydropyrine 3-methyl-5-3-(4,4-diphenyl-1-piperidinyl)-propyl-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-piridine-3,5-dicarboxylate-hydrochloride (niguldipine)1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-l-tyrosyl]-4-phenylpiperazine12-O-tetradecanoyl-phorbol-13-acetate2-chloro-(ε-amino-Lys(75))-[6-(4-(N,N′-diethylaminophenyl)-1,3,5-triazin-4-yl]-CaM adduct3′-(β-chloroethyl)-2′,4′-dioxo-3,5′-spiro-oxazolidino-4-deacetoxy-vinblastine7,12-dimethylbenz[a]anthraceneApoptosisAutophagyB859-35CAPP(1)-CaMCa(2+) binding proteinCalmodulinCancer biologyCell proliferationDMBAEBBFL-CaMFPCEHBCHBCPJ-8KAR-2KN-62KN-93N-(4-aminobutyl)-2-naphthalenesulfonamideN-(4-aminobutyl)-5-chloro-2-naphthalenesulfonamideN-(6-aminohexyl)-1-naphthalenesulfonamideN-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamideN-8-aminooctyl-5-iodo-naphthalenesulfonamideN-[2-[N-(4-chlorocinnamyl)-N-methylaminomethyl]phenyl]-N-(2-hydroxyethyl)-4-methoxybenzenesulfonamideO-(4-ethoxyl-butyl)-berbamineRITC-CaMTA-CaMTFPTPAW-12W-13W-5W-7fluorescein-CaM adductfluphenazine-N-2-chloroethanenorchlorpromazine-CaM adductrhodamine isothiocyanate-CaM adducttrifluoperazine

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