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Published on: August 23, 2019

A new strategy to block tumor growth by inhibiting endocannabinoid inactivation

Maurizio Bifulco1, Chiara Laezza, Marta Valenti

  • 1Istituto di Endocrinologia ed Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare L. Califano, Università di Napoli Federico II, Italy. maubiful@unina.it

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|August 4, 2004
PubMed

Insights

Inhibiting the breakdown of endocannabinoids, natural compounds that regulate cell growth, slowed the growth of rat thyroid tumors. These findings suggest that drugs targeting endocannabinoid inactivation could be new anti-cancer therapies.

Area of Science:

  • Oncology
  • Endocrinology
  • Pharmacology

Background:

  • Endocannabinoid signaling is elevated in many cancers, potentially inhibiting tumor cell proliferation.
  • Understanding the role of endocannabinoids in cancer progression is crucial for developing new therapeutic strategies.

Purpose of the Study:

  • To investigate the impact of inhibiting endocannabinoid degradation on rat thyroid tumor xenograft growth in vivo.
  • To explore the potential of endocannabinoid inactivation inhibitors as anti-cancer agents.

Main Methods:

  • Utilized VDM-11 (a cellular re-uptake inhibitor) and arachidonoyl-serotonin (AA-5-HT, an enzymatic hydrolysis blocker) to inhibit endocannabinoid degradation.
  • Assessed tumor growth in athymic mice bearing rat thyroid tumor xenografts.
  • Measured endocannabinoid concentrations in excised tumors.
  • Evaluated the effects of endocannabinoids, VDM-11, AA-5-HT, and the CB1 antagonist SR141716A on transformed rat thyroid cells in vitro and in vivo.

Main Results:

  • Both VDM-11 and AA-5-HT significantly inhibited the in vivo growth of rat thyroid tumor xenografts.
  • Tumors from treated mice showed significantly higher endocannabinoid concentrations.
  • Endocannabinoids, VDM-11, and AA-5-HT inhibited the in vitro proliferation of transformed rat thyroid cells.
  • The anti-proliferative effects were partially reversed by the CB1 receptor antagonist SR141716A.
  • SR141716A alone showed a slight inhibitory effect on tumor cell growth both in vitro and in vivo.

Conclusions:

  • Endocannabinoids play a tonic role in controlling tumor growth in vivo through both CB1-mediated and non-CB1-mediated pathways.
  • Inhibitors of endocannabinoid inactivation represent a promising avenue for the development of novel anti-cancer therapeutics, regardless of the specific anti-proliferative mechanism.

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