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Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro
Osteosarcoma strikes hundreds of people each year, of both advanced and younger ages, and is often terminal. Like many tumor types, these bone tumors will frequently undergo a neuroendocrine transition, utilizing autocrine and/or paracrine hormones as growth factors and/or promoters of angiogenesis...
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Published in: | BMC cancer 2019-02, Vol.19 (1), p.158-158, Article 158 |
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description | Osteosarcoma strikes hundreds of people each year, of both advanced and younger ages, and is often terminal. Like many tumor types, these bone tumors will frequently undergo a neuroendocrine transition, utilizing autocrine and/or paracrine hormones as growth factors and/or promoters of angiogenesis to facilitate progression and metastasis. While many of these factors and their actions on tumor growth are characterized, some tumor-derived neuropeptides remain unexplored.
Using validated canine osteosarcoma cell lines in vitro, as well as cells derived from spontaneous tumors in dogs, we explored the autocrine production of two neuropeptides typically found in the hypothalamus, and most closely associated with reproduction: gonadotropin-releasing hormone (GnRH) and kisspeptin (Kiss-1). We evaluated gene expression and protein secretion of these hormones using quantitative RT-PCR and a sensitive radioimmunoassay, and explored changes in cell proliferation determined by MTS cell viability assays.
Our current studies reveal that several canine osteosarcoma cell lines (COS, POS, HMPOS, D17, C4) synthesize and secrete GnRH and express the GnRH receptor, while COS and POS also express kiss1 and its cognate receptor. We have further found that GnRH and kisspeptin, exogenously applied to these tumor cells, exert significant effects on both gene expression and proliferation. Of particular interest, kisspeptin exposure stimulated GnRH secretion from COS, similarly to the functional relationship observed within the neuroendocrine reproductive axis. Additionally, GnRH and kisspeptin treatment both increased COS proliferation, which additionally manifested in increased expression of the bone remodeling ligand rankl within these cells. These effects were blocked by treatment with a specific GnRH receptor inhibitor. Both neuropeptides were found to increase expression of the specific serotonin (5HT) receptor htr2a, the activation of which has previously been associated with cellular proliferation, suggesting that production of these factors by osteosarcoma cells may act to sensitize tumors to circulating 5HT of local and/or enteric origin.
Here we report that kisspeptin and GnRH act as autocrine growth factors in canine osteosarcoma cells in vitro, modulating RANKL and serotonin receptor expression in a manner consistent with pro-proliferative effects. Pharmacological targeting of these hormones may represent new avenues of osteosarcoma treatment. |
doi_str_mv | 10.1186/s12885-019-5363-4 |
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Using validated canine osteosarcoma cell lines in vitro, as well as cells derived from spontaneous tumors in dogs, we explored the autocrine production of two neuropeptides typically found in the hypothalamus, and most closely associated with reproduction: gonadotropin-releasing hormone (GnRH) and kisspeptin (Kiss-1). We evaluated gene expression and protein secretion of these hormones using quantitative RT-PCR and a sensitive radioimmunoassay, and explored changes in cell proliferation determined by MTS cell viability assays.
Our current studies reveal that several canine osteosarcoma cell lines (COS, POS, HMPOS, D17, C4) synthesize and secrete GnRH and express the GnRH receptor, while COS and POS also express kiss1 and its cognate receptor. We have further found that GnRH and kisspeptin, exogenously applied to these tumor cells, exert significant effects on both gene expression and proliferation. Of particular interest, kisspeptin exposure stimulated GnRH secretion from COS, similarly to the functional relationship observed within the neuroendocrine reproductive axis. Additionally, GnRH and kisspeptin treatment both increased COS proliferation, which additionally manifested in increased expression of the bone remodeling ligand rankl within these cells. These effects were blocked by treatment with a specific GnRH receptor inhibitor. Both neuropeptides were found to increase expression of the specific serotonin (5HT) receptor htr2a, the activation of which has previously been associated with cellular proliferation, suggesting that production of these factors by osteosarcoma cells may act to sensitize tumors to circulating 5HT of local and/or enteric origin.
Here we report that kisspeptin and GnRH act as autocrine growth factors in canine osteosarcoma cells in vitro, modulating RANKL and serotonin receptor expression in a manner consistent with pro-proliferative effects. Pharmacological targeting of these hormones may represent new avenues of osteosarcoma treatment.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/s12885-019-5363-4</identifier><identifier>PMID: 30777054</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Angiogenesis ; Autocrine ; Autocrine signalling ; Bone cancer ; Bone remodeling ; Bone tumors ; Breast cancer ; Cell adhesion & migration ; Cell growth ; Cell proliferation ; Colorectal cancer ; Gene expression ; GnRH ; Gonadotropin-releasing hormone ; Gonadotropins ; Growth factors ; Hormones ; Hypothalamus ; Kinases ; Kiss1 protein ; Kisspeptin ; Ligands ; Medical prognosis ; Metastases ; Metastasis ; Neuropeptides ; Osteosarcoma ; Osteosarcoma cells ; Paracrine signalling ; Pituitary (anterior) ; Polymerase chain reaction ; Proliferation ; Proteins ; Radioimmunoassay ; Sarcoma ; Secretion ; Serotonin ; TRANCE protein ; Tumor cells ; Tumors</subject><ispartof>BMC cancer, 2019-02, Vol.19 (1), p.158-158, Article 158</ispartof><rights>COPYRIGHT 2019 BioMed Central Ltd.</rights><rights>Copyright © 2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s). 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c625t-bec1304a351a8ac4e9a94633e15ef1f8108a3799475ce9ca622b78de354837a13</citedby><cites>FETCH-LOGICAL-c625t-bec1304a351a8ac4e9a94633e15ef1f8108a3799475ce9ca622b78de354837a13</cites><orcidid>0000-0002-8634-4933</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379937/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2183395246?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,25734,27905,27906,36993,36994,44571,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30777054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weinman, Marcus A</creatorcontrib><creatorcontrib>Fischer, Jacob A</creatorcontrib><creatorcontrib>Jacobs, Dakota C</creatorcontrib><creatorcontrib>Goodall, Cheri P</creatorcontrib><creatorcontrib>Bracha, Shay</creatorcontrib><creatorcontrib>Chappell, Patrick E</creatorcontrib><title>Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>Osteosarcoma strikes hundreds of people each year, of both advanced and younger ages, and is often terminal. Like many tumor types, these bone tumors will frequently undergo a neuroendocrine transition, utilizing autocrine and/or paracrine hormones as growth factors and/or promoters of angiogenesis to facilitate progression and metastasis. While many of these factors and their actions on tumor growth are characterized, some tumor-derived neuropeptides remain unexplored.
Using validated canine osteosarcoma cell lines in vitro, as well as cells derived from spontaneous tumors in dogs, we explored the autocrine production of two neuropeptides typically found in the hypothalamus, and most closely associated with reproduction: gonadotropin-releasing hormone (GnRH) and kisspeptin (Kiss-1). We evaluated gene expression and protein secretion of these hormones using quantitative RT-PCR and a sensitive radioimmunoassay, and explored changes in cell proliferation determined by MTS cell viability assays.
Our current studies reveal that several canine osteosarcoma cell lines (COS, POS, HMPOS, D17, C4) synthesize and secrete GnRH and express the GnRH receptor, while COS and POS also express kiss1 and its cognate receptor. We have further found that GnRH and kisspeptin, exogenously applied to these tumor cells, exert significant effects on both gene expression and proliferation. Of particular interest, kisspeptin exposure stimulated GnRH secretion from COS, similarly to the functional relationship observed within the neuroendocrine reproductive axis. Additionally, GnRH and kisspeptin treatment both increased COS proliferation, which additionally manifested in increased expression of the bone remodeling ligand rankl within these cells. These effects were blocked by treatment with a specific GnRH receptor inhibitor. Both neuropeptides were found to increase expression of the specific serotonin (5HT) receptor htr2a, the activation of which has previously been associated with cellular proliferation, suggesting that production of these factors by osteosarcoma cells may act to sensitize tumors to circulating 5HT of local and/or enteric origin.
Here we report that kisspeptin and GnRH act as autocrine growth factors in canine osteosarcoma cells in vitro, modulating RANKL and serotonin receptor expression in a manner consistent with pro-proliferative effects. Pharmacological targeting of these hormones may represent new avenues of osteosarcoma treatment.</description><subject>Angiogenesis</subject><subject>Autocrine</subject><subject>Autocrine signalling</subject><subject>Bone cancer</subject><subject>Bone remodeling</subject><subject>Bone tumors</subject><subject>Breast cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Gene expression</subject><subject>GnRH</subject><subject>Gonadotropin-releasing hormone</subject><subject>Gonadotropins</subject><subject>Growth factors</subject><subject>Hormones</subject><subject>Hypothalamus</subject><subject>Kinases</subject><subject>Kiss1 protein</subject><subject>Kisspeptin</subject><subject>Ligands</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Neuropeptides</subject><subject>Osteosarcoma</subject><subject>Osteosarcoma cells</subject><subject>Paracrine signalling</subject><subject>Pituitary (anterior)</subject><subject>Polymerase chain reaction</subject><subject>Proliferation</subject><subject>Proteins</subject><subject>Radioimmunoassay</subject><subject>Sarcoma</subject><subject>Secretion</subject><subject>Serotonin</subject><subject>TRANCE protein</subject><subject>Tumor cells</subject><subject>Tumors</subject><issn>1471-2407</issn><issn>1471-2407</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkl2L1DAUhoso7jr6A7yRgiB60TVpkia9EYbFj4EFwY_rcCY9ncnQNmOSDuu_N93ZWaciuUhy8rxvksObZS8puaJUVe8DLZUSBaF1IVjFCv4ou6Rc0qLkRD4-W19kz0LYEUKlIuppdsGIlJIIfpn1yzE64-2A-d67ZjTRuiF3be7xtD9gDrc25AOO3u1xH22DIYe2RRPDpOpsix5OQgPD5OZCRBfAG9dDbof8YKN3z7MnLXQBX9zPi-znp48_rr8UN18_r66XN4WpShGLNRrKCAcmKCgwHGuoecUYUoEtbRUlCpisay6FwdpAVZZrqRpkgismgbJFtjr6Ng52eu9tD_63dmD1XcH5jQYfrelQ0yQXogRaipIzyRThpgVWCal4LZp18vpw9NqP6x4bg0P00M1M5yeD3eqNO-hqemJyXGRv7w28-zViiLq3wWDXwYBuDLqkilW8LiVJ6Ot_0J0b_ZBadUexOr2x-kttIH3ADq1L95rJVC-FoqxSouKJuvoPlUaDvTVuwNam-kzwbiZITMTbuIExBL36_m3Ovjljtwhd3AbXjVMIwhykR9B4F4LH9qFxlOgpxPoYYp1CrKcQ60nz6rzjD4pTatkfWtbrVw</recordid><startdate>20190218</startdate><enddate>20190218</enddate><creator>Weinman, Marcus A</creator><creator>Fischer, Jacob A</creator><creator>Jacobs, Dakota C</creator><creator>Goodall, Cheri P</creator><creator>Bracha, Shay</creator><creator>Chappell, Patrick E</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-8634-4933</orcidid></search><sort><creationdate>20190218</creationdate><title>Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro</title><author>Weinman, Marcus A ; Fischer, Jacob A ; Jacobs, Dakota C ; Goodall, Cheri P ; Bracha, Shay ; Chappell, Patrick E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c625t-bec1304a351a8ac4e9a94633e15ef1f8108a3799475ce9ca622b78de354837a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Angiogenesis</topic><topic>Autocrine</topic><topic>Autocrine signalling</topic><topic>Bone cancer</topic><topic>Bone remodeling</topic><topic>Bone tumors</topic><topic>Breast cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Colorectal cancer</topic><topic>Gene expression</topic><topic>GnRH</topic><topic>Gonadotropin-releasing hormone</topic><topic>Gonadotropins</topic><topic>Growth factors</topic><topic>Hormones</topic><topic>Hypothalamus</topic><topic>Kinases</topic><topic>Kiss1 protein</topic><topic>Kisspeptin</topic><topic>Ligands</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Neuropeptides</topic><topic>Osteosarcoma</topic><topic>Osteosarcoma cells</topic><topic>Paracrine signalling</topic><topic>Pituitary (anterior)</topic><topic>Polymerase chain reaction</topic><topic>Proliferation</topic><topic>Proteins</topic><topic>Radioimmunoassay</topic><topic>Sarcoma</topic><topic>Secretion</topic><topic>Serotonin</topic><topic>TRANCE protein</topic><topic>Tumor cells</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weinman, Marcus A</creatorcontrib><creatorcontrib>Fischer, Jacob A</creatorcontrib><creatorcontrib>Jacobs, Dakota C</creatorcontrib><creatorcontrib>Goodall, Cheri P</creatorcontrib><creatorcontrib>Bracha, Shay</creatorcontrib><creatorcontrib>Chappell, Patrick E</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weinman, Marcus A</au><au>Fischer, Jacob A</au><au>Jacobs, Dakota C</au><au>Goodall, Cheri P</au><au>Bracha, Shay</au><au>Chappell, Patrick E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2019-02-18</date><risdate>2019</risdate><volume>19</volume><issue>1</issue><spage>158</spage><epage>158</epage><pages>158-158</pages><artnum>158</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>Osteosarcoma strikes hundreds of people each year, of both advanced and younger ages, and is often terminal. Like many tumor types, these bone tumors will frequently undergo a neuroendocrine transition, utilizing autocrine and/or paracrine hormones as growth factors and/or promoters of angiogenesis to facilitate progression and metastasis. While many of these factors and their actions on tumor growth are characterized, some tumor-derived neuropeptides remain unexplored.
Using validated canine osteosarcoma cell lines in vitro, as well as cells derived from spontaneous tumors in dogs, we explored the autocrine production of two neuropeptides typically found in the hypothalamus, and most closely associated with reproduction: gonadotropin-releasing hormone (GnRH) and kisspeptin (Kiss-1). We evaluated gene expression and protein secretion of these hormones using quantitative RT-PCR and a sensitive radioimmunoassay, and explored changes in cell proliferation determined by MTS cell viability assays.
Our current studies reveal that several canine osteosarcoma cell lines (COS, POS, HMPOS, D17, C4) synthesize and secrete GnRH and express the GnRH receptor, while COS and POS also express kiss1 and its cognate receptor. We have further found that GnRH and kisspeptin, exogenously applied to these tumor cells, exert significant effects on both gene expression and proliferation. Of particular interest, kisspeptin exposure stimulated GnRH secretion from COS, similarly to the functional relationship observed within the neuroendocrine reproductive axis. Additionally, GnRH and kisspeptin treatment both increased COS proliferation, which additionally manifested in increased expression of the bone remodeling ligand rankl within these cells. These effects were blocked by treatment with a specific GnRH receptor inhibitor. Both neuropeptides were found to increase expression of the specific serotonin (5HT) receptor htr2a, the activation of which has previously been associated with cellular proliferation, suggesting that production of these factors by osteosarcoma cells may act to sensitize tumors to circulating 5HT of local and/or enteric origin.
Here we report that kisspeptin and GnRH act as autocrine growth factors in canine osteosarcoma cells in vitro, modulating RANKL and serotonin receptor expression in a manner consistent with pro-proliferative effects. Pharmacological targeting of these hormones may represent new avenues of osteosarcoma treatment.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>30777054</pmid><doi>10.1186/s12885-019-5363-4</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-8634-4933</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Angiogenesis Autocrine Autocrine signalling Bone cancer Bone remodeling Bone tumors Breast cancer Cell adhesion & migration Cell growth Cell proliferation Colorectal cancer Gene expression GnRH Gonadotropin-releasing hormone Gonadotropins Growth factors Hormones Hypothalamus Kinases Kiss1 protein Kisspeptin Ligands Medical prognosis Metastases Metastasis Neuropeptides Osteosarcoma Osteosarcoma cells Paracrine signalling Pituitary (anterior) Polymerase chain reaction Proliferation Proteins Radioimmunoassay Sarcoma Secretion Serotonin TRANCE protein Tumor cells Tumors |
title | Autocrine production of reproductive axis neuropeptides affects proliferation of canine osteosarcoma in vitro |
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