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RPSAP52 lncRNA is overexpressed in pituitary tumors and promotes cell proliferation by acting as miRNA sponge for HMGA proteins
Long non-coding RNAs (lncRNAs) are emerging as fundamental players in cancer biology. Indeed, they are deregulated in several neoplasias and have been associated with cancer progression, tumor recurrence, and resistance to treatment, thus representing potential biomarkers for cancer diagnosis, progn...
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| Published in: | Journal of molecular medicine (Berlin, Germany) Germany), 2019-07, Vol.97 (7), p.1019-1032 |
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| container_issue | 7 |
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| container_title | Journal of molecular medicine (Berlin, Germany) |
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| creator | D’Angelo, Daniela Mussnich, Paula Sepe, Romina Raia, Maddalena del Vecchio, Luigi Cappabianca, Paolo Pellecchia, Simona Petrosino, Sara Saggio, Serena Solari, Domenico Fraggetta, Filippo Fusco, Alfredo |
| description | Long non-coding RNAs (lncRNAs) are emerging as fundamental players in cancer biology. Indeed, they are deregulated in several neoplasias and have been associated with cancer progression, tumor recurrence, and resistance to treatment, thus representing potential biomarkers for cancer diagnosis, prognosis, and therapy. In this study, we aimed to identify lncRNAs associated with pituitary tumorigenesis
.
We have analyzed the lncRNA expression profile of a panel of gonadotroph pituitary adenomas in comparison with normal pituitaries. Then, we focused on RPSAP52, a novel lncRNA antisense for the
HMGA2
gene, whose overexpression plays a critical role in the development of pituitary adenomas. We report that RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues. Conversely, its expression showed a variable behavior in somatotroph adenomas. We also demonstrate that RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2. Interestingly, RPSAP52 also positively modulates HMGA1, the other member of the High-Mobility Group A family. Moreover, functional studies indicate that RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle. The results reported here reveal a novel mechanism, based on the overexpression of the lncRNA RPSAP52, which contributes to pituitary tumorigenesis, and propose this lncRNA as a novel player in the development of these tumors.
Key Messages
RPSAP52 is overexpressed in pituitary adenomas.
RPSAP52 increases HMGA protein levels.
A ceRNA mechanism is proposed for the increased HMGA1/2 expression. |
| doi_str_mv | 10.1007/s00109-019-01789-7 |
| format | article |
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.
We have analyzed the lncRNA expression profile of a panel of gonadotroph pituitary adenomas in comparison with normal pituitaries. Then, we focused on RPSAP52, a novel lncRNA antisense for the
HMGA2
gene, whose overexpression plays a critical role in the development of pituitary adenomas. We report that RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues. Conversely, its expression showed a variable behavior in somatotroph adenomas. We also demonstrate that RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2. Interestingly, RPSAP52 also positively modulates HMGA1, the other member of the High-Mobility Group A family. Moreover, functional studies indicate that RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle. The results reported here reveal a novel mechanism, based on the overexpression of the lncRNA RPSAP52, which contributes to pituitary tumorigenesis, and propose this lncRNA as a novel player in the development of these tumors.
Key Messages
RPSAP52 is overexpressed in pituitary adenomas.
RPSAP52 increases HMGA protein levels.
A ceRNA mechanism is proposed for the increased HMGA1/2 expression.</description><identifier>ISSN: 0946-2716</identifier><identifier>EISSN: 1432-1440</identifier><identifier>DOI: 10.1007/s00109-019-01789-7</identifier><identifier>PMID: 31076808</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Antisense therapy ; Base Sequence ; Binding Sites - genetics ; Biomedical and Life Sciences ; Biomedicine ; Brain cancer ; Brain tumors ; Cancer ; Cell cycle ; Cell Cycle - genetics ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Cell Proliferation - genetics ; Gene Expression Regulation, Neoplastic ; HMGA Proteins - metabolism ; Human Genetics ; Humans ; Internal Medicine ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Molecular Medicine ; Mutation - genetics ; Original Article ; Pituitary ; Pituitary (anterior) ; Pituitary gland ; Pituitary Neoplasms - genetics ; Pituitary Neoplasms - pathology ; Prolactin ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Tumorigenesis ; Tumors</subject><ispartof>Journal of molecular medicine (Berlin, Germany), 2019-07, Vol.97 (7), p.1019-1032</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Journal of Molecular Medicine is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-4c22881a0217f359a189e59ed5ca16989205bd1096ee4d9b150464757010dd943</citedby><cites>FETCH-LOGICAL-c375t-4c22881a0217f359a189e59ed5ca16989205bd1096ee4d9b150464757010dd943</cites><orcidid>0000-0001-8865-0347</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31076808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>D’Angelo, Daniela</creatorcontrib><creatorcontrib>Mussnich, Paula</creatorcontrib><creatorcontrib>Sepe, Romina</creatorcontrib><creatorcontrib>Raia, Maddalena</creatorcontrib><creatorcontrib>del Vecchio, Luigi</creatorcontrib><creatorcontrib>Cappabianca, Paolo</creatorcontrib><creatorcontrib>Pellecchia, Simona</creatorcontrib><creatorcontrib>Petrosino, Sara</creatorcontrib><creatorcontrib>Saggio, Serena</creatorcontrib><creatorcontrib>Solari, Domenico</creatorcontrib><creatorcontrib>Fraggetta, Filippo</creatorcontrib><creatorcontrib>Fusco, Alfredo</creatorcontrib><title>RPSAP52 lncRNA is overexpressed in pituitary tumors and promotes cell proliferation by acting as miRNA sponge for HMGA proteins</title><title>Journal of molecular medicine (Berlin, Germany)</title><addtitle>J Mol Med</addtitle><addtitle>J Mol Med (Berl)</addtitle><description>Long non-coding RNAs (lncRNAs) are emerging as fundamental players in cancer biology. Indeed, they are deregulated in several neoplasias and have been associated with cancer progression, tumor recurrence, and resistance to treatment, thus representing potential biomarkers for cancer diagnosis, prognosis, and therapy. In this study, we aimed to identify lncRNAs associated with pituitary tumorigenesis
.
We have analyzed the lncRNA expression profile of a panel of gonadotroph pituitary adenomas in comparison with normal pituitaries. Then, we focused on RPSAP52, a novel lncRNA antisense for the
HMGA2
gene, whose overexpression plays a critical role in the development of pituitary adenomas. We report that RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues. Conversely, its expression showed a variable behavior in somatotroph adenomas. We also demonstrate that RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2. Interestingly, RPSAP52 also positively modulates HMGA1, the other member of the High-Mobility Group A family. Moreover, functional studies indicate that RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle. The results reported here reveal a novel mechanism, based on the overexpression of the lncRNA RPSAP52, which contributes to pituitary tumorigenesis, and propose this lncRNA as a novel player in the development of these tumors.
Key Messages
RPSAP52 is overexpressed in pituitary adenomas.
RPSAP52 increases HMGA protein levels.
A ceRNA mechanism is proposed for the increased HMGA1/2 expression.</description><subject>Antisense therapy</subject><subject>Base Sequence</subject><subject>Binding Sites - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell Cycle - genetics</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>HMGA Proteins - metabolism</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Molecular Medicine</subject><subject>Mutation - genetics</subject><subject>Original Article</subject><subject>Pituitary</subject><subject>Pituitary (anterior)</subject><subject>Pituitary gland</subject><subject>Pituitary Neoplasms - genetics</subject><subject>Pituitary Neoplasms - pathology</subject><subject>Prolactin</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>0946-2716</issn><issn>1432-1440</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNp9kUFvFSEUhYnR2Gf1D7gwJG7cjAIDw7B8aWprUtum6prwZu40NDMwchljV_3rZXxVky66IITw3XNPziHkLWcfOWP6EzLGmakYX49uTaWfkQ2Xtai4lOw52TAjm0po3hyQV4g3BdfKyJfkoOZMNy1rN-Tu6vLb9lIJOobu6nxLPdL4CxL8nhMgQk99oLPPi88u3dK8TDEhdaGnc4pTzIC0g3FcX6MfILnsY6C7W-q67MM1dUgnv-riHMM10CEmevr1ZLsOZPABX5MXgxsR3jzch-TH5-PvR6fV2cXJl6PtWdXVWuVKdkK0LXdMcD3UyjjeGlAGetU53pjWCKZ2fUmjAZC92XHFZCO10iWhvjeyPiQf9rpl8c8FMNvJ42rdBYgLWiFqbjhr5Yq-f4TexCWF4q5QxUZTN7otlNhTXYqICQY7Jz-VkCxndq3H7uuxpR77px6ry9C7B-llN0H_b-RvHwWo9wCWrxJY-r_7Cdl787aZUw</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>D’Angelo, Daniela</creator><creator>Mussnich, Paula</creator><creator>Sepe, Romina</creator><creator>Raia, Maddalena</creator><creator>del Vecchio, Luigi</creator><creator>Cappabianca, Paolo</creator><creator>Pellecchia, Simona</creator><creator>Petrosino, Sara</creator><creator>Saggio, Serena</creator><creator>Solari, Domenico</creator><creator>Fraggetta, Filippo</creator><creator>Fusco, Alfredo</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature 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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8865-0347</orcidid></search><sort><creationdate>20190701</creationdate><title>RPSAP52 lncRNA is overexpressed in pituitary tumors and promotes cell proliferation by acting as miRNA sponge for HMGA proteins</title><author>D’Angelo, Daniela ; Mussnich, Paula ; Sepe, Romina ; Raia, Maddalena ; del Vecchio, Luigi ; Cappabianca, Paolo ; Pellecchia, Simona ; Petrosino, Sara ; Saggio, Serena ; Solari, Domenico ; Fraggetta, Filippo ; Fusco, Alfredo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-4c22881a0217f359a189e59ed5ca16989205bd1096ee4d9b150464757010dd943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antisense therapy</topic><topic>Base Sequence</topic><topic>Binding Sites - genetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain cancer</topic><topic>Brain tumors</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell Cycle - genetics</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>HMGA Proteins - metabolism</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Molecular Medicine</topic><topic>Mutation - genetics</topic><topic>Original Article</topic><topic>Pituitary</topic><topic>Pituitary (anterior)</topic><topic>Pituitary gland</topic><topic>Pituitary Neoplasms - genetics</topic><topic>Pituitary Neoplasms - pathology</topic><topic>Prolactin</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>D’Angelo, Daniela</creatorcontrib><creatorcontrib>Mussnich, Paula</creatorcontrib><creatorcontrib>Sepe, Romina</creatorcontrib><creatorcontrib>Raia, Maddalena</creatorcontrib><creatorcontrib>del Vecchio, Luigi</creatorcontrib><creatorcontrib>Cappabianca, Paolo</creatorcontrib><creatorcontrib>Pellecchia, Simona</creatorcontrib><creatorcontrib>Petrosino, Sara</creatorcontrib><creatorcontrib>Saggio, Serena</creatorcontrib><creatorcontrib>Solari, Domenico</creatorcontrib><creatorcontrib>Fraggetta, Filippo</creatorcontrib><creatorcontrib>Fusco, Alfredo</creatorcontrib><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>Neurosciences Abstracts</collection><collection>ProQuest - 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Academic</collection><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>D’Angelo, Daniela</au><au>Mussnich, Paula</au><au>Sepe, Romina</au><au>Raia, Maddalena</au><au>del Vecchio, Luigi</au><au>Cappabianca, Paolo</au><au>Pellecchia, Simona</au><au>Petrosino, Sara</au><au>Saggio, Serena</au><au>Solari, Domenico</au><au>Fraggetta, Filippo</au><au>Fusco, Alfredo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RPSAP52 lncRNA is overexpressed in pituitary tumors and promotes cell proliferation by acting as miRNA sponge for HMGA proteins</atitle><jtitle>Journal of molecular medicine (Berlin, Germany)</jtitle><stitle>J Mol Med</stitle><addtitle>J Mol Med (Berl)</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>97</volume><issue>7</issue><spage>1019</spage><epage>1032</epage><pages>1019-1032</pages><issn>0946-2716</issn><eissn>1432-1440</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Long non-coding RNAs (lncRNAs) are emerging as fundamental players in cancer biology. Indeed, they are deregulated in several neoplasias and have been associated with cancer progression, tumor recurrence, and resistance to treatment, thus representing potential biomarkers for cancer diagnosis, prognosis, and therapy. In this study, we aimed to identify lncRNAs associated with pituitary tumorigenesis
.
We have analyzed the lncRNA expression profile of a panel of gonadotroph pituitary adenomas in comparison with normal pituitaries. Then, we focused on RPSAP52, a novel lncRNA antisense for the
HMGA2
gene, whose overexpression plays a critical role in the development of pituitary adenomas. We report that RPSAP52 expression is highly upregulated in gonadotroph and prolactin-secreting pituitary adenomas, where it correlates with that of HMGA2, compared with normal pituitary tissues. Conversely, its expression showed a variable behavior in somatotroph adenomas. We also demonstrate that RPSAP52 enhances HMGA2 protein expression in a ceRNA-dependent way acting as sponge for miR-15a, miR-15b, and miR-16, which have been already described to be able to target HMGA2. Interestingly, RPSAP52 also positively modulates HMGA1, the other member of the High-Mobility Group A family. Moreover, functional studies indicate that RPSAP52 promotes cell growth by enhancing the G1-S transition of the cell cycle. The results reported here reveal a novel mechanism, based on the overexpression of the lncRNA RPSAP52, which contributes to pituitary tumorigenesis, and propose this lncRNA as a novel player in the development of these tumors.
Key Messages
RPSAP52 is overexpressed in pituitary adenomas.
RPSAP52 increases HMGA protein levels.
A ceRNA mechanism is proposed for the increased HMGA1/2 expression.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31076808</pmid><doi>10.1007/s00109-019-01789-7</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-8865-0347</orcidid></addata></record> |
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| ispartof | Journal of molecular medicine (Berlin, Germany), 2019-07, Vol.97 (7), p.1019-1032 |
| issn | 0946-2716 1432-1440 |
| language | eng |
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| subjects | Antisense therapy Base Sequence Binding Sites - genetics Biomedical and Life Sciences Biomedicine Brain cancer Brain tumors Cancer Cell cycle Cell Cycle - genetics Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - genetics Gene Expression Regulation, Neoplastic HMGA Proteins - metabolism Human Genetics Humans Internal Medicine MicroRNAs - genetics MicroRNAs - metabolism miRNA Molecular Medicine Mutation - genetics Original Article Pituitary Pituitary (anterior) Pituitary gland Pituitary Neoplasms - genetics Pituitary Neoplasms - pathology Prolactin RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Tumorigenesis Tumors |
| title | RPSAP52 lncRNA is overexpressed in pituitary tumors and promotes cell proliferation by acting as miRNA sponge for HMGA proteins |
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