The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells

GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2,...
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Autor*in:	Mikhail G. Akimov [verfasserIn] Natalia M. Gretskaya [verfasserIn] Polina V. Dudina [verfasserIn] Galina D. Sherstyanykh [verfasserIn] Galina N. Zinchenko [verfasserIn] Oksana V. Serova [verfasserIn] Ksenia O. Degtyaryova [verfasserIn] Igor E. Deyev [verfasserIn] Vladimir V. Bezuglov [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 24(2023), 6, p 5524
Übergeordnetes Werk:	volume:24 ; year:2023 ; number:6, p 5524

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms24065524

Katalog-ID:	DOAJ087340496

Internformat


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700	0		\|a Natalia M. Gretskaya \|e verfasserin \|4 aut
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author_variant	m g a mga n m g nmg p v d pvd g d s gds g n z gnz o v s ovs k o d kod i e d ied v v b vvb
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allfields	10.3390/ijms24065524 doi (DE-627)DOAJ087340496 (DE-599)DOAJ9d6728718ffa40d0b335f24f8962224d DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mikhail G. Akimov verfasserin aut The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55. CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry Natalia M. Gretskaya verfasserin aut Polina V. Dudina verfasserin aut Galina D. Sherstyanykh verfasserin aut Galina N. Zinchenko verfasserin aut Oksana V. Serova verfasserin aut Ksenia O. Degtyaryova verfasserin aut Igor E. Deyev verfasserin aut Vladimir V. Bezuglov verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 6, p 5524 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:6, p 5524 https://doi.org/10.3390/ijms24065524 kostenfrei https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d kostenfrei https://www.mdpi.com/1422-0067/24/6/5524 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 6, p 5524
spelling	10.3390/ijms24065524 doi (DE-627)DOAJ087340496 (DE-599)DOAJ9d6728718ffa40d0b335f24f8962224d DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mikhail G. Akimov verfasserin aut The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55. CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry Natalia M. Gretskaya verfasserin aut Polina V. Dudina verfasserin aut Galina D. Sherstyanykh verfasserin aut Galina N. Zinchenko verfasserin aut Oksana V. Serova verfasserin aut Ksenia O. Degtyaryova verfasserin aut Igor E. Deyev verfasserin aut Vladimir V. Bezuglov verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 6, p 5524 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:6, p 5524 https://doi.org/10.3390/ijms24065524 kostenfrei https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d kostenfrei https://www.mdpi.com/1422-0067/24/6/5524 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 6, p 5524
allfields_unstemmed	10.3390/ijms24065524 doi (DE-627)DOAJ087340496 (DE-599)DOAJ9d6728718ffa40d0b335f24f8962224d DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mikhail G. Akimov verfasserin aut The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55. CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry Natalia M. Gretskaya verfasserin aut Polina V. Dudina verfasserin aut Galina D. Sherstyanykh verfasserin aut Galina N. Zinchenko verfasserin aut Oksana V. Serova verfasserin aut Ksenia O. Degtyaryova verfasserin aut Igor E. Deyev verfasserin aut Vladimir V. Bezuglov verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 6, p 5524 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:6, p 5524 https://doi.org/10.3390/ijms24065524 kostenfrei https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d kostenfrei https://www.mdpi.com/1422-0067/24/6/5524 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 6, p 5524
allfieldsGer	10.3390/ijms24065524 doi (DE-627)DOAJ087340496 (DE-599)DOAJ9d6728718ffa40d0b335f24f8962224d DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mikhail G. Akimov verfasserin aut The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55. CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry Natalia M. Gretskaya verfasserin aut Polina V. Dudina verfasserin aut Galina D. Sherstyanykh verfasserin aut Galina N. Zinchenko verfasserin aut Oksana V. Serova verfasserin aut Ksenia O. Degtyaryova verfasserin aut Igor E. Deyev verfasserin aut Vladimir V. Bezuglov verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 6, p 5524 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:6, p 5524 https://doi.org/10.3390/ijms24065524 kostenfrei https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d kostenfrei https://www.mdpi.com/1422-0067/24/6/5524 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 6, p 5524
allfieldsSound	10.3390/ijms24065524 doi (DE-627)DOAJ087340496 (DE-599)DOAJ9d6728718ffa40d0b335f24f8962224d DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Mikhail G. Akimov verfasserin aut The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55. CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry Natalia M. Gretskaya verfasserin aut Polina V. Dudina verfasserin aut Galina D. Sherstyanykh verfasserin aut Galina N. Zinchenko verfasserin aut Oksana V. Serova verfasserin aut Ksenia O. Degtyaryova verfasserin aut Igor E. Deyev verfasserin aut Vladimir V. Bezuglov verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 24(2023), 6, p 5524 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:24 year:2023 number:6, p 5524 https://doi.org/10.3390/ijms24065524 kostenfrei https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d kostenfrei https://www.mdpi.com/1422-0067/24/6/5524 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 24 2023 6, p 5524
language	English
source	In International Journal of Molecular Sciences 24(2023), 6, p 5524 volume:24 year:2023 number:6, p 5524
sourceStr	In International Journal of Molecular Sciences 24(2023), 6, p 5524 volume:24 year:2023 number:6, p 5524
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Mikhail G. Akimov @@aut@@ Natalia M. Gretskaya @@aut@@ Polina V. Dudina @@aut@@ Galina D. Sherstyanykh @@aut@@ Galina N. Zinchenko @@aut@@ Oksana V. Serova @@aut@@ Ksenia O. Degtyaryova @@aut@@ Igor E. Deyev @@aut@@ Vladimir V. Bezuglov @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ087340496
language_de	englisch
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callnumber-first	Q - Science
author	Mikhail G. Akimov
spellingShingle	Mikhail G. Akimov misc QH301-705.5 misc QD1-999 misc CB1 misc CB2 misc GPR18 misc GPR55-CB2 heterodimers misc GPR55 functional selectivity misc GPR55 proliferation stimulation misc Biology (General) misc Chemistry The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells
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topic_title	QH301-705.5 QD1-999 The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells CB1 CB2 GPR18 GPR55-CB2 heterodimers GPR55 functional selectivity GPR55 proliferation stimulation
topic	misc QH301-705.5 misc QD1-999 misc CB1 misc CB2 misc GPR18 misc GPR55-CB2 heterodimers misc GPR55 functional selectivity misc GPR55 proliferation stimulation misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc CB1 misc CB2 misc GPR18 misc GPR55-CB2 heterodimers misc GPR55 functional selectivity misc GPR55 proliferation stimulation misc Biology (General) misc Chemistry
topic_browse	misc QH301-705.5 misc QD1-999 misc CB1 misc CB2 misc GPR18 misc GPR55-CB2 heterodimers misc GPR55 functional selectivity misc GPR55 proliferation stimulation misc Biology (General) misc Chemistry
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title	The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells
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title_full	The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells
author_sort	Mikhail G. Akimov
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author_browse	Mikhail G. Akimov Natalia M. Gretskaya Polina V. Dudina Galina D. Sherstyanykh Galina N. Zinchenko Oksana V. Serova Ksenia O. Degtyaryova Igor E. Deyev Vladimir V. Bezuglov
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author-letter	Mikhail G. Akimov
doi_str_mv	10.3390/ijms24065524
author2-role	verfasserin
title_sort	mechanisms of gpr55 receptor functional selectivity during apoptosis and proliferation regulation in cancer cells
callnumber	QH301-705.5
title_auth	The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells
abstract	GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55.
abstractGer	GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55.
abstract_unstemmed	GPR55 is a non-canonical cannabinoid receptor, important for cancer proliferation. Depending on the ligand, it induces either cell proliferation or death. The objective of the study was to establish the mechanisms of this multidirectional signaling. Using the CRISPR-Cas9 system, the GPR55, CB1, CB2, and GPR18 receptor knockouts of the MDA-MB-231 line were obtained. After the CB2 receptor knockout, the pro-apoptotic activity of the pro-apoptotic ligand docosahexaenoyl dopamine (DHA-DA) slightly increased, while the pro-proliferative activity of the most active synthetic ligand of the GPR55 receptor (ML-184) completely disappeared. On the original cell line, the stimulatory effect of ML-184 was removed by the CB2 receptor blocker and by GPR55 receptor knockout. Thus, it can be confidently assumed that when proliferation is stimulated with the participation of the GPR55 receptor, a signal is transmitted from the CB2 receptor to the GPR55 receptor due to the formation of a heterodimer. GPR18 was additionally involved in the implementation of the pro-apoptotic effect of DHA-DA, while the CB1 receptor is not involved. In the implementation of the pro-apoptotic action of DHA-DA, the elimination of Gα<sub<13</sub< led to a decrease in cytotoxicity. The obtained data provide novel details to the mechanism of the pro-proliferative action of GPR55.
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container_issue	6, p 5524
title_short	The Mechanisms of GPR55 Receptor Functional Selectivity during Apoptosis and Proliferation Regulation in Cancer Cells
url	https://doi.org/10.3390/ijms24065524 https://doaj.org/article/9d6728718ffa40d0b335f24f8962224d https://www.mdpi.com/1422-0067/24/6/5524 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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author2	Natalia M. Gretskaya Polina V. Dudina Galina D. Sherstyanykh Galina N. Zinchenko Oksana V. Serova Ksenia O. Degtyaryova Igor E. Deyev Vladimir V. Bezuglov
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