GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis
G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we re...
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| Veröffentlicht in: | Scientific reports 2019-09, Vol.9 (1), p.13902-15, Article 13902 |
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| description | G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown. GRK2-K220R (kinase dead) and GRK2-S670A (unphosphorylated, constitutively active) conferred protection from cisplatin that was similar to wildtype GRK2, suggesting that this protection may be mediated though a kinase-independent activity of GRK2. These data demonstrate that GRK2 contributes to proliferation and survival of these medulloblastoma cell lines and to their protection from cisplatin- and etoposide-induced apoptosis. |
| doi_str_mv | 10.1038/s41598-019-50157-5 |
| format | Article |
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However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown. GRK2-K220R (kinase dead) and GRK2-S670A (unphosphorylated, constitutively active) conferred protection from cisplatin that was similar to wildtype GRK2, suggesting that this protection may be mediated though a kinase-independent activity of GRK2. These data demonstrate that GRK2 contributes to proliferation and survival of these medulloblastoma cell lines and to their protection from cisplatin- and etoposide-induced apoptosis.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-50157-5</identifier><identifier>PMID: 31554835</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/106 ; 13/109 ; 13/2 ; 13/31 ; 13/95 ; 42/35 ; 42/89 ; 631/67 ; 631/80 ; 82/29 ; AKT protein ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; b-Adrenergic-receptor kinase ; Brain cancer ; Cell Proliferation - drug effects ; Cell Proliferation - physiology ; Cell survival ; Cerebellar Neoplasms - drug therapy ; Cerebellar Neoplasms - metabolism ; Chemotherapy ; Cisplatin ; Cisplatin - pharmacology ; Etoposide ; Etoposide - pharmacology ; Extracellular signal-regulated kinase ; G protein-coupled receptors ; G-Protein-Coupled Receptor Kinase 2 - metabolism ; HEK293 Cells ; Humanities and Social Sciences ; Humans ; Medulloblastoma ; Medulloblastoma - drug therapy ; Medulloblastoma - metabolism ; multidisciplinary ; Phosphorylation ; Phosphorylation - drug effects ; Science ; Science (multidisciplinary)</subject><ispartof>Scientific reports, 2019-09, Vol.9 (1), p.13902-15, Article 13902</ispartof><rights>The Author(s) 2019</rights><rights>2019. 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However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown. GRK2-K220R (kinase dead) and GRK2-S670A (unphosphorylated, constitutively active) conferred protection from cisplatin that was similar to wildtype GRK2, suggesting that this protection may be mediated though a kinase-independent activity of GRK2. 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drug effects</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pathania, Anup S.</creatorcontrib><creatorcontrib>Ren, Xiuhai</creatorcontrib><creatorcontrib>Mahdi, Min Y.</creatorcontrib><creatorcontrib>Shackleford, Gregory M.</creatorcontrib><creatorcontrib>Erdreich-Epstein, Anat</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pathania, Anup S.</au><au>Ren, Xiuhai</au><au>Mahdi, Min Y.</au><au>Shackleford, Gregory M.</au><au>Erdreich-Epstein, Anat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-09-25</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>13902</spage><epage>15</epage><pages>13902-15</pages><artnum>13902</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown. GRK2-K220R (kinase dead) and GRK2-S670A (unphosphorylated, constitutively active) conferred protection from cisplatin that was similar to wildtype GRK2, suggesting that this protection may be mediated though a kinase-independent activity of GRK2. These data demonstrate that GRK2 contributes to proliferation and survival of these medulloblastoma cell lines and to their protection from cisplatin- and etoposide-induced apoptosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31554835</pmid><doi>10.1038/s41598-019-50157-5</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-4269-4373</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13/1 13/106 13/109 13/2 13/31 13/95 42/35 42/89 631/67 631/80 82/29 AKT protein Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Apoptosis - physiology b-Adrenergic-receptor kinase Brain cancer Cell Proliferation - drug effects Cell Proliferation - physiology Cell survival Cerebellar Neoplasms - drug therapy Cerebellar Neoplasms - metabolism Chemotherapy Cisplatin Cisplatin - pharmacology Etoposide Etoposide - pharmacology Extracellular signal-regulated kinase G protein-coupled receptors G-Protein-Coupled Receptor Kinase 2 - metabolism HEK293 Cells Humanities and Social Sciences Humans Medulloblastoma Medulloblastoma - drug therapy Medulloblastoma - metabolism multidisciplinary Phosphorylation Phosphorylation - drug effects Science Science (multidisciplinary) |
| title | GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis |
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