GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells
Recent studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a key molecule in sustaining androgen-mediated prostate cancer cell survival. Thus, the aim of this study was to determine whether 20-HETE can affect the metastatic potential of androgen-insensitive prostate cancer cells, an...
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| Veröffentlicht in: | Biochimica et biophysica acta. Molecular and cell biology of lipids 2020-02, Vol.1865 (2), p.158573-158573, Article 158573 |
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| container_title | Biochimica et biophysica acta. Molecular and cell biology of lipids |
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| creator | Cárdenas, Sofia Colombero, Cecilia Panelo, Laura Dakarapu, Rambabu Falck, John R. Costas, Monica A. Nowicki, Susana |
| description | Recent studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a key molecule in sustaining androgen-mediated prostate cancer cell survival. Thus, the aim of this study was to determine whether 20-HETE can affect the metastatic potential of androgen-insensitive prostate cancer cells, and the implication of the newly described 20-HETE receptor, GPR75, in mediating these effects.
The expression of GPR75, protein phosphorylation, actin polymerization and protein distribution were assessed by western blot and/or fluorescence microscopy. Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells.
20-HETE (0.1 nM) promoted the acquisition of a mesenchymal phenotype by increasing EMT, the release of MMP-2, cell migration and invasion, actin stress fiber formation and anchorage-independent growth. Also, 20-HETE augmented the expression of HIC-5, the phosphorylation of EGFR, NF-κB, AKT and p-38 and the intracellular redistribution of p-AKT and PKCα. These effects were impaired by GPR75 antagonism and/or silencing. Accordingly, the inhibition of 20-HETE formation with N-hydroxy-N′-(4-n-butyl-2-methylphenyl) formamidine (HET0016) elicited the opposite effects.
The present results show for the first time the involvement of the 20-HETE-GPR75 receptor in the activation of intracellular signaling known to be stimulated in cell malignant transformations leading to the differentiation of PC-3 cells towards a more aggressive phenotype. Targeting the 20-HETE/GPR75 pathway is a promising and novel approach to interfere with prostate tumor cell malignant progression.
[Display omitted]
•Androgen-insensitive prostate cancer cells (PC-3) express the 20-HETE receptor, GPR75.•Stimulation of GPR75 by 20-HETE increases metastatic features of PC-3 cells.•The inhibition of 20-HETE synthesis diminished metastatic features of PC-3 cells.•20-HETE-GPR75 triggered signaling pathways involved in cell malignant transformation. |
| doi_str_mv | 10.1016/j.bbalip.2019.158573 |
| format | Article |
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The expression of GPR75, protein phosphorylation, actin polymerization and protein distribution were assessed by western blot and/or fluorescence microscopy. Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells.
20-HETE (0.1 nM) promoted the acquisition of a mesenchymal phenotype by increasing EMT, the release of MMP-2, cell migration and invasion, actin stress fiber formation and anchorage-independent growth. Also, 20-HETE augmented the expression of HIC-5, the phosphorylation of EGFR, NF-κB, AKT and p-38 and the intracellular redistribution of p-AKT and PKCα. These effects were impaired by GPR75 antagonism and/or silencing. Accordingly, the inhibition of 20-HETE formation with N-hydroxy-N′-(4-n-butyl-2-methylphenyl) formamidine (HET0016) elicited the opposite effects.
The present results show for the first time the involvement of the 20-HETE-GPR75 receptor in the activation of intracellular signaling known to be stimulated in cell malignant transformations leading to the differentiation of PC-3 cells towards a more aggressive phenotype. Targeting the 20-HETE/GPR75 pathway is a promising and novel approach to interfere with prostate tumor cell malignant progression.
[Display omitted]
•Androgen-insensitive prostate cancer cells (PC-3) express the 20-HETE receptor, GPR75.•Stimulation of GPR75 by 20-HETE increases metastatic features of PC-3 cells.•The inhibition of 20-HETE synthesis diminished metastatic features of PC-3 cells.•20-HETE-GPR75 triggered signaling pathways involved in cell malignant transformation.</description><identifier>ISSN: 1388-1981</identifier><identifier>EISSN: 1879-2618</identifier><identifier>DOI: 10.1016/j.bbalip.2019.158573</identifier><identifier>PMID: 31760076</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>20-HETE ; actin ; agar ; agonists ; Amidines - pharmacology ; Androgens - metabolism ; antagonists ; Arachidonic acid metabolites ; cell movement ; Cell Movement - drug effects ; cell viability ; Epithelial-Mesenchymal Transition - drug effects ; fluorescence microscopy ; Gene Knockdown Techniques ; gene silencing ; GPR75 receptor ; Humans ; Hydroxyeicosatetraenoic Acids - agonists ; Hydroxyeicosatetraenoic Acids - antagonists & inhibitors ; Hydroxyeicosatetraenoic Acids - metabolism ; in vitro studies ; Intracellular Signaling Peptides and Proteins - metabolism ; LIM Domain Proteins - metabolism ; Male ; Matrix Metalloproteinase 2 - metabolism ; Metastasis ; neoplasm cells ; PC-3 Cells ; phenotype ; polymerization ; Prostate cancer ; prostatic neoplasms ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - pathology ; protein kinase C ; protein phosphorylation ; Receptors, G-Protein-Coupled - antagonists & inhibitors ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - metabolism ; RNA, Small Interfering - metabolism ; Signal Transduction - drug effects ; tissue repair ; transcription factor NF-kappa B ; Western blotting</subject><ispartof>Biochimica et biophysica acta. Molecular and cell biology of lipids, 2020-02, Vol.1865 (2), p.158573-158573, Article 158573</ispartof><rights>2019 Elsevier B.V.</rights><rights>Copyright © 2019 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-e701cc491db8aaf6cf21e20ed690809832d19a501528338655144c27ea47cea13</citedby><cites>FETCH-LOGICAL-c496t-e701cc491db8aaf6cf21e20ed690809832d19a501528338655144c27ea47cea13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1388198119302240$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31760076$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cárdenas, Sofia</creatorcontrib><creatorcontrib>Colombero, Cecilia</creatorcontrib><creatorcontrib>Panelo, Laura</creatorcontrib><creatorcontrib>Dakarapu, Rambabu</creatorcontrib><creatorcontrib>Falck, John R.</creatorcontrib><creatorcontrib>Costas, Monica A.</creatorcontrib><creatorcontrib>Nowicki, Susana</creatorcontrib><title>GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells</title><title>Biochimica et biophysica acta. Molecular and cell biology of lipids</title><addtitle>Biochim Biophys Acta Mol Cell Biol Lipids</addtitle><description>Recent studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a key molecule in sustaining androgen-mediated prostate cancer cell survival. Thus, the aim of this study was to determine whether 20-HETE can affect the metastatic potential of androgen-insensitive prostate cancer cells, and the implication of the newly described 20-HETE receptor, GPR75, in mediating these effects.
The expression of GPR75, protein phosphorylation, actin polymerization and protein distribution were assessed by western blot and/or fluorescence microscopy. Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells.
20-HETE (0.1 nM) promoted the acquisition of a mesenchymal phenotype by increasing EMT, the release of MMP-2, cell migration and invasion, actin stress fiber formation and anchorage-independent growth. Also, 20-HETE augmented the expression of HIC-5, the phosphorylation of EGFR, NF-κB, AKT and p-38 and the intracellular redistribution of p-AKT and PKCα. These effects were impaired by GPR75 antagonism and/or silencing. Accordingly, the inhibition of 20-HETE formation with N-hydroxy-N′-(4-n-butyl-2-methylphenyl) formamidine (HET0016) elicited the opposite effects.
The present results show for the first time the involvement of the 20-HETE-GPR75 receptor in the activation of intracellular signaling known to be stimulated in cell malignant transformations leading to the differentiation of PC-3 cells towards a more aggressive phenotype. Targeting the 20-HETE/GPR75 pathway is a promising and novel approach to interfere with prostate tumor cell malignant progression.
[Display omitted]
•Androgen-insensitive prostate cancer cells (PC-3) express the 20-HETE receptor, GPR75.•Stimulation of GPR75 by 20-HETE increases metastatic features of PC-3 cells.•The inhibition of 20-HETE synthesis diminished metastatic features of PC-3 cells.•20-HETE-GPR75 triggered signaling pathways involved in cell malignant transformation.</description><subject>20-HETE</subject><subject>actin</subject><subject>agar</subject><subject>agonists</subject><subject>Amidines - pharmacology</subject><subject>Androgens - metabolism</subject><subject>antagonists</subject><subject>Arachidonic acid metabolites</subject><subject>cell movement</subject><subject>Cell Movement - drug effects</subject><subject>cell viability</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>fluorescence microscopy</subject><subject>Gene Knockdown Techniques</subject><subject>gene silencing</subject><subject>GPR75 receptor</subject><subject>Humans</subject><subject>Hydroxyeicosatetraenoic Acids - agonists</subject><subject>Hydroxyeicosatetraenoic Acids - antagonists & inhibitors</subject><subject>Hydroxyeicosatetraenoic Acids - metabolism</subject><subject>in vitro studies</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>LIM Domain Proteins - metabolism</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Metastasis</subject><subject>neoplasm cells</subject><subject>PC-3 Cells</subject><subject>phenotype</subject><subject>polymerization</subject><subject>Prostate cancer</subject><subject>prostatic neoplasms</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - pathology</subject><subject>protein kinase C</subject><subject>protein phosphorylation</subject><subject>Receptors, G-Protein-Coupled - antagonists & inhibitors</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>tissue repair</subject><subject>transcription factor NF-kappa B</subject><subject>Western blotting</subject><issn>1388-1981</issn><issn>1879-2618</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNUV1rFDEUHUSxtfoPRObRl1lzk8nXiyBlbQsFRepzyGburFlmkzHJLvTfm2FrtS_iUy6cc8_NOadp3gJZAQHxYbfabOzk5xUloFfAFZfsWXMOSuqOClDP68yU6kArOGte5bwjBDhj_GVzxkAKQqQ4b-LV12-StwkdziWmdo-DtwVzS0l3vb5bd9lvQz0Ttq0NQ4WLzcUW79oRbTmkyozjAqW4xdD5kDFkX_wR2znFhYqts8Fhah1OU37dvBjtlPHNw3vRfP-8vru87m6_XN1cfrrtXK9F6VAScHWEYaOsHYUbKSAlOAhNFNGK0QG05dUQVYwpwTn0vaMSbS8dWmAXzceT7nzYVE8OQ0l2MnPye5vuTbTePEWC_2G28WiE5lIKXQXePwik-POAuZi9z4sFGzAesqE9gxq5YP9BrXFrrginldqfqK6GkxOOjz8CYpZazc6cajVLreZUa11797ebx6XfPf6xizXTo8dksvNYYx98rbaYIfp_X_gFGSu2SQ</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Cárdenas, Sofia</creator><creator>Colombero, Cecilia</creator><creator>Panelo, Laura</creator><creator>Dakarapu, Rambabu</creator><creator>Falck, John R.</creator><creator>Costas, Monica A.</creator><creator>Nowicki, Susana</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20200201</creationdate><title>GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells</title><author>Cárdenas, Sofia ; Colombero, Cecilia ; Panelo, Laura ; Dakarapu, Rambabu ; Falck, John R. ; Costas, Monica A. ; Nowicki, Susana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-e701cc491db8aaf6cf21e20ed690809832d19a501528338655144c27ea47cea13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>20-HETE</topic><topic>actin</topic><topic>agar</topic><topic>agonists</topic><topic>Amidines - pharmacology</topic><topic>Androgens - metabolism</topic><topic>antagonists</topic><topic>Arachidonic acid metabolites</topic><topic>cell movement</topic><topic>Cell Movement - drug effects</topic><topic>cell viability</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>fluorescence microscopy</topic><topic>Gene Knockdown Techniques</topic><topic>gene silencing</topic><topic>GPR75 receptor</topic><topic>Humans</topic><topic>Hydroxyeicosatetraenoic Acids - agonists</topic><topic>Hydroxyeicosatetraenoic Acids - antagonists & inhibitors</topic><topic>Hydroxyeicosatetraenoic Acids - metabolism</topic><topic>in vitro studies</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>LIM Domain Proteins - metabolism</topic><topic>Male</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Metastasis</topic><topic>neoplasm cells</topic><topic>PC-3 Cells</topic><topic>phenotype</topic><topic>polymerization</topic><topic>Prostate cancer</topic><topic>prostatic neoplasms</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - pathology</topic><topic>protein kinase C</topic><topic>protein phosphorylation</topic><topic>Receptors, G-Protein-Coupled - antagonists & inhibitors</topic><topic>Receptors, G-Protein-Coupled - genetics</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>tissue repair</topic><topic>transcription factor NF-kappa B</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cárdenas, Sofia</creatorcontrib><creatorcontrib>Colombero, Cecilia</creatorcontrib><creatorcontrib>Panelo, Laura</creatorcontrib><creatorcontrib>Dakarapu, Rambabu</creatorcontrib><creatorcontrib>Falck, John R.</creatorcontrib><creatorcontrib>Costas, Monica A.</creatorcontrib><creatorcontrib>Nowicki, Susana</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biochimica et biophysica acta. Molecular and cell biology of lipids</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cárdenas, Sofia</au><au>Colombero, Cecilia</au><au>Panelo, Laura</au><au>Dakarapu, Rambabu</au><au>Falck, John R.</au><au>Costas, Monica A.</au><au>Nowicki, Susana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells</atitle><jtitle>Biochimica et biophysica acta. Molecular and cell biology of lipids</jtitle><addtitle>Biochim Biophys Acta Mol Cell Biol Lipids</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>1865</volume><issue>2</issue><spage>158573</spage><epage>158573</epage><pages>158573-158573</pages><artnum>158573</artnum><issn>1388-1981</issn><eissn>1879-2618</eissn><abstract>Recent studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a key molecule in sustaining androgen-mediated prostate cancer cell survival. Thus, the aim of this study was to determine whether 20-HETE can affect the metastatic potential of androgen-insensitive prostate cancer cells, and the implication of the newly described 20-HETE receptor, GPR75, in mediating these effects.
The expression of GPR75, protein phosphorylation, actin polymerization and protein distribution were assessed by western blot and/or fluorescence microscopy. Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells.
20-HETE (0.1 nM) promoted the acquisition of a mesenchymal phenotype by increasing EMT, the release of MMP-2, cell migration and invasion, actin stress fiber formation and anchorage-independent growth. Also, 20-HETE augmented the expression of HIC-5, the phosphorylation of EGFR, NF-κB, AKT and p-38 and the intracellular redistribution of p-AKT and PKCα. These effects were impaired by GPR75 antagonism and/or silencing. Accordingly, the inhibition of 20-HETE formation with N-hydroxy-N′-(4-n-butyl-2-methylphenyl) formamidine (HET0016) elicited the opposite effects.
The present results show for the first time the involvement of the 20-HETE-GPR75 receptor in the activation of intracellular signaling known to be stimulated in cell malignant transformations leading to the differentiation of PC-3 cells towards a more aggressive phenotype. Targeting the 20-HETE/GPR75 pathway is a promising and novel approach to interfere with prostate tumor cell malignant progression.
[Display omitted]
•Androgen-insensitive prostate cancer cells (PC-3) express the 20-HETE receptor, GPR75.•Stimulation of GPR75 by 20-HETE increases metastatic features of PC-3 cells.•The inhibition of 20-HETE synthesis diminished metastatic features of PC-3 cells.•20-HETE-GPR75 triggered signaling pathways involved in cell malignant transformation.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>31760076</pmid><doi>10.1016/j.bbalip.2019.158573</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Biochimica et biophysica acta. Molecular and cell biology of lipids, 2020-02, Vol.1865 (2), p.158573-158573, Article 158573 |
| issn | 1388-1981 1879-2618 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 20-HETE actin agar agonists Amidines - pharmacology Androgens - metabolism antagonists Arachidonic acid metabolites cell movement Cell Movement - drug effects cell viability Epithelial-Mesenchymal Transition - drug effects fluorescence microscopy Gene Knockdown Techniques gene silencing GPR75 receptor Humans Hydroxyeicosatetraenoic Acids - agonists Hydroxyeicosatetraenoic Acids - antagonists & inhibitors Hydroxyeicosatetraenoic Acids - metabolism in vitro studies Intracellular Signaling Peptides and Proteins - metabolism LIM Domain Proteins - metabolism Male Matrix Metalloproteinase 2 - metabolism Metastasis neoplasm cells PC-3 Cells phenotype polymerization Prostate cancer prostatic neoplasms Prostatic Neoplasms - drug therapy Prostatic Neoplasms - pathology protein kinase C protein phosphorylation Receptors, G-Protein-Coupled - antagonists & inhibitors Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - metabolism RNA, Small Interfering - metabolism Signal Transduction - drug effects tissue repair transcription factor NF-kappa B Western blotting |
| title | GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells |
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