Please use this identifier to cite or link to this item: http://dx.doi.org/10.25673/113483
Title: Elucidation of GPR55-associated signaling behind THC and LPI reducing effects on Ki67-immunoreactive nuclei in patient-derived glioblastoma cells
Author(s): Kolbe, Marc Richard
Hohmann, TimLook up in the Integrated Authority File of the German National Library
Hohmann, UrszulaLook up in the Integrated Authority File of the German National Library
Maronde, ErikLook up in the Integrated Authority File of the German National Library
Golbik, RalphLook up in the Integrated Authority File of the German National Library
Prell, Julian
Illert, Jörg
Strauss, Christian
Dehghani, FaramarzLook up in the Integrated Authority File of the German National Library
Issue Date: 2023
Type: Article
Language: English
Abstract: GPR55 is involved in many physiological and pathological processes. In cancer, GPR55 has been described to show accelerating and decelerating effects in tumor progression resulting from distinct intracellular signaling pathways. GPR55 becomes activated by LPI and various plant-derived, endogenous, and synthetic cannabinoids. Cannabinoids such as THC exerted antitumor effects by inhibiting tumor cell proliferation or inducing apoptosis. Besides its effects through CB1 and CB2 receptors, THC modulates cellular responses among others via GPR55. Previously, we reported a reduction in Ki67-immunoreactive nuclei of human glioblastoma cells after GPR55 activation in general by THC and in particular by LPI. In the present study, we investigated intracellular mechanisms leading to an altered number of Ki67+ nuclei after stimulation of GPR55 by LPI and THC. Pharmacological analyses revealed a strongly involved PLC-IP3 signaling and cell-type-specific differences in Gα-, Gβγ-, RhoA-ROCK, and calcineurin signaling. Furthermore, immunochemical visualization of the calcineurin-dependent transcription factor NFAT revealed an unchanged subcellular localization after THC or LPI treatment. The data underline the cell-type-specific diversity of GPR55-associated signaling pathways in coupling to intracellular G proteins. Furthermore, this diversity might determine the outcome and the individual responsiveness of tumor cells to GPR55 stimulation by cannabin oids.
URI: https://opendata.uni-halle.de//handle/1981185920/115438
http://dx.doi.org/10.25673/113483
Open Access: Open access publication
License: (CC BY 4.0) Creative Commons Attribution 4.0(CC BY 4.0) Creative Commons Attribution 4.0
Journal Title: Cells
Publisher: MDPI
Publisher Place: Basel
Volume: 12
Issue: 22
Original Publication: 10.3390/cells12222646
Page Start: 1
Page End: 26
Appears in Collections:Open Access Publikationen der MLU

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