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  • Short Communication
  • Open Access

Cannabinoid receptor activation inhibits cell cycle progression by modulating 14-3-3β

Cellular & Molecular Biology LettersAn International Journal201419:200

  • Received: 10 December 2013
  • Accepted: 1 July 2014
  • Published:


Cannabinoids display various pharmacological activities, including tumor regression, anti-inflammatory and neuroprotective effects. To investigate the molecular mechanisms underlying the pharmacological effects of cannabinoids, we used a yeast two-hybrid system to screen a mouse brain cDNA library for proteins interacting with type 1 cannabinoid receptor (CB1R). Using the intracellular loop 3 of CB1R as bait, we identified 14-3-3β as an interacting partner of CB1R and confirmed their interaction using affinity-binding assays. 14-3-3β has been reported to induce a cell cycle delay at the G2/M phase. We tested the effects of cannabinoids on cell cycle progression in HeLa cells synchronized using a double-thymidine block-and-release protocol and found an increase in the population of G2/M phase cells. We further found that CB1R activation augmented the interaction of 14-3-3β with Wee1 and Cdc25B, and promoted phosphorylation of Cdc2 at Tyr-15. These results suggest that cannabinoids induce cell cycle delay at the G2/M phase by activating 14-3-3β.


  • Cannabinoids
  • Cdc2
  • Cdc25B
  • Cyclin B
  • G2/M phase
  • GIPs
  • HeLa
  • Phosphorylation
  • Wee1
  • Yeast-two hybrid