Non-Canonical Cannabinoid Receptors with Distinct Binding and Signaling Properties in Prostate and Other Cancer Cell Types Mediate Cell Death

Shoeib, Amal; Benson, Lance N.; Mu, Shengyu; MacMillan-Crow, Lee Ann; Prather, Paul L.

doi:10.3390/ijms23063049

Cited by 1 publication

(1 citation statement)

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“…[ 9 ] Mounting evidence suggests activation of cannabinoid receptors is associated with inhibition of tumorigenesis and progress in multiple tumor models. [ 10 , 11 , 12 ] For example, CB1 activation by the selective agonist arachidonoyl 2′‐chloroethylamide (ACEA) could suppress the proliferation, migration, and invasion of colorectal cancer cells. Tumor‐associated macrophages (TAMs) are important cellular components of tumor‐infiltrating immune cells in TME.…”

Section: Introductionmentioning

confidence: 99%

Molecular Engineering of Electrosprayed Hydrogel Microspheres to Achieve Synergistic Anti‐Tumor Chemo‐Immunotherapy with ACEA Cargo

Deng,

Li,

Tao

et al. 2024

Advanced Science

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Molecular engineering of drug delivering platforms to provide collaborative biological effects with loaded drugs is of great medical significance. Herein, cannabinoid receptor 1 (CB1)‐ and reactive oxygen species (ROS)‐targeting electrosprayed microspheres (MSs) are fabricated by loading with the CB1 agonist arachidonoyl 2′‐chloroethylamide (ACEA) and producing ROS in a photoresponsive manner. The synergistic anti‐tumor effects of ACEA and ROS released from the MSs are assessed. ACEA inhibits epidermal growth factor receptor signaling and altered tumor microenvironment (TME) by activating CB1 to induce tumor cell death. The MSs are composed of glycidyl methacrylate‐conjugated xanthan gum (XGMA) and Fe3+, which form dual molecular networks based on a Fe3+‐(COO−)3 network and a C═C addition reaction network. Interestingly, the Fe3+‐(COO−)3 network can be disassembled instantly under the conditions of lactate sodium and ultraviolet exposure, and the disassembly is accompanied by massive ROS production, which directly injures tumor cells. Meanwhile, the transition of dual networks to a single network boosts the ACEA release. Together, the activities of the ACEA and MSs promote immunogenic tumor cell death and create a tumor‐suppressive TME by increasing M1‐like tumor‐associated macrophages and CD8+ T cells. In summation, this study demonstrates strong prospects of improving anti‐tumor effects of drug delivering platforms through molecular design.

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