LRIG1 negatively regulates RET mutants and is downregulated in thyroid cancer
Papillary thyroid carcinoma (PTC) and medullary thyroid carcinoma (MTC) are characterized by genomic rearrangements and point mutations in the proto-oncogene RET. Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1...
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| Veröffentlicht in: | International journal of oncology 2018-04, Vol.52 (4), p.1189-1197 |
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| container_title | International journal of oncology |
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| creator | Lindquist, David Alsina, Fernando C Herdenberg, Carl Larsson, Catharina Höppener, Jo Wang, Na Paratcha, Gustavo Tarján, Miklós Tot, Tibor Henriksson, Roger Hedman, Håkan |
| description | Papillary thyroid carcinoma (PTC) and medullary thyroid carcinoma (MTC) are characterized by genomic rearrangements and point mutations in the proto-oncogene RET. Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1 expression levels are associated with patient survival in many cancer types. In the present study, we investigated whether the oncogenic RET mutants RET2A (C634R) and RET2B (M918T) were regulated by LRIG1, and the possible effects of LRIG1 expression in thyroid cancer were investigated in three different clinical cohorts and in a RET2B-driven mouse model of MTC. LRIG1 was shown to physically interact with both RET2A and RET2B and to restrict their ligand-independent activation. LRIG1 mRNA levels were downregulated in PTC and MTC compared to normal thyroid gland tissue. There was no apparent association between LRIG1 RNA or protein expression levels and patient survival in the studied cohorts. The transgenic RET2B mice developed pre-cancerous medullary thyroid lesions at a high frequency (36%); however, no overt cancers were observed. There was no significant difference in the incidence of pre-cancerous lesions between Lrig1 wild-type and Lrig1-deficient RET2B mice. In conclusion, the findings that LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in PTC and MTC may suggest that LRIG1 functions as a thyroid tumor suppressor. |
| doi_str_mv | 10.3892/ijo.2018.4273 |
| format | Article |
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Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1 expression levels are associated with patient survival in many cancer types. In the present study, we investigated whether the oncogenic RET mutants RET2A (C634R) and RET2B (M918T) were regulated by LRIG1, and the possible effects of LRIG1 expression in thyroid cancer were investigated in three different clinical cohorts and in a RET2B-driven mouse model of MTC. LRIG1 was shown to physically interact with both RET2A and RET2B and to restrict their ligand-independent activation. LRIG1 mRNA levels were downregulated in PTC and MTC compared to normal thyroid gland tissue. There was no apparent association between LRIG1 RNA or protein expression levels and patient survival in the studied cohorts. The transgenic RET2B mice developed pre-cancerous medullary thyroid lesions at a high frequency (36%); however, no overt cancers were observed. There was no significant difference in the incidence of pre-cancerous lesions between Lrig1 wild-type and Lrig1-deficient RET2B mice. In conclusion, the findings that LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in PTC and MTC may suggest that LRIG1 functions as a thyroid tumor suppressor.</description><identifier>ISSN: 1019-6439</identifier><identifier>ISSN: 1791-2423</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2018.4273</identifier><identifier>PMID: 29436694</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Analysis ; Animals ; C634R ; Carcinoma, Neuroendocrine - genetics ; Carcinoma, Neuroendocrine - metabolism ; Carcinoma, Papillary - genetics ; Carcinoma, Papillary - metabolism ; Care and treatment ; Development and progression ; Down-Regulation ; Gene expression ; Gene Expression Regulation, Neoplastic - genetics ; Gene mutation ; Genetic aspects ; Health aspects ; Humans ; LRIG1 ; M918T ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; MEN2A ; MEN2B ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation ; Oncology ; onkologi ; Proto-Oncogene Proteins c-ret - genetics ; Proto-Oncogene Proteins c-ret - metabolism ; RET ; Rodents ; Studies ; Thyroid cancer ; Thyroid Neoplasms - genetics ; Thyroid Neoplasms - metabolism ; Tumor suppressor genes</subject><ispartof>International journal of oncology, 2018-04, Vol.52 (4), p.1189-1197</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Lindquist et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c589t-ee9084a85eb6a1efd647fa992cef31bce043526c0d43960a3cd60818c1a66cbc3</citedby><cites>FETCH-LOGICAL-c589t-ee9084a85eb6a1efd647fa992cef31bce043526c0d43960a3cd60818c1a66cbc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,550,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29436694$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-145641$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:137828367$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Lindquist, David</creatorcontrib><creatorcontrib>Alsina, Fernando C</creatorcontrib><creatorcontrib>Herdenberg, Carl</creatorcontrib><creatorcontrib>Larsson, Catharina</creatorcontrib><creatorcontrib>Höppener, Jo</creatorcontrib><creatorcontrib>Wang, Na</creatorcontrib><creatorcontrib>Paratcha, Gustavo</creatorcontrib><creatorcontrib>Tarján, Miklós</creatorcontrib><creatorcontrib>Tot, Tibor</creatorcontrib><creatorcontrib>Henriksson, Roger</creatorcontrib><creatorcontrib>Hedman, Håkan</creatorcontrib><title>LRIG1 negatively regulates RET mutants and is downregulated in thyroid cancer</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Papillary thyroid carcinoma (PTC) and medullary thyroid carcinoma (MTC) are characterized by genomic rearrangements and point mutations in the proto-oncogene RET. Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1 expression levels are associated with patient survival in many cancer types. In the present study, we investigated whether the oncogenic RET mutants RET2A (C634R) and RET2B (M918T) were regulated by LRIG1, and the possible effects of LRIG1 expression in thyroid cancer were investigated in three different clinical cohorts and in a RET2B-driven mouse model of MTC. LRIG1 was shown to physically interact with both RET2A and RET2B and to restrict their ligand-independent activation. LRIG1 mRNA levels were downregulated in PTC and MTC compared to normal thyroid gland tissue. There was no apparent association between LRIG1 RNA or protein expression levels and patient survival in the studied cohorts. The transgenic RET2B mice developed pre-cancerous medullary thyroid lesions at a high frequency (36%); however, no overt cancers were observed. There was no significant difference in the incidence of pre-cancerous lesions between Lrig1 wild-type and Lrig1-deficient RET2B mice. In conclusion, the findings that LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in PTC and MTC may suggest that LRIG1 functions as a thyroid tumor suppressor.</description><subject>Analysis</subject><subject>Animals</subject><subject>C634R</subject><subject>Carcinoma, Neuroendocrine - genetics</subject><subject>Carcinoma, Neuroendocrine - metabolism</subject><subject>Carcinoma, Papillary - genetics</subject><subject>Carcinoma, Papillary - metabolism</subject><subject>Care and treatment</subject><subject>Development and progression</subject><subject>Down-Regulation</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene mutation</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>LRIG1</subject><subject>M918T</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>MEN2A</subject><subject>MEN2B</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Mutation</subject><subject>Oncology</subject><subject>onkologi</subject><subject>Proto-Oncogene Proteins c-ret - genetics</subject><subject>Proto-Oncogene Proteins c-ret - metabolism</subject><subject>RET</subject><subject>Rodents</subject><subject>Studies</subject><subject>Thyroid cancer</subject><subject>Thyroid Neoplasms - genetics</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Tumor suppressor genes</subject><issn>1019-6439</issn><issn>1791-2423</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>D8T</sourceid><recordid>eNp9kt9rFDEQxxdRbD199FUWBN_2zO9LXoSj1lo4EUr1NeSys3s5d5OaZFvuvzdHr7UHInnIMPnMl5nJt6reYjSnUpGPbhvmBGE5Z2RBn1WneKFwQxihz0uMsGoEo-qkepXSFiHCOcIvqxOiGBVCsdPq2-rq8gLXHnqT3S0MuzpCPw0mQ6qvzq_rccrG51Qb39Yu1W248w9ASfg6b3YxuLa2xluIr6sXnRkSvDncs-rHl_Prs6_N6vvF5dly1VguVW4AFJLMSA5rYTB0rWCLzihFLHQUry0gRjkRFrWld4EMta1AEkuLjRB2bemsau510x3cTGt9E91o4k4H4_Qh9atEoJlCnOL_8p_dz6UOsdfTOGnMuGB7_tM9X-ARWgs-RzMclR2_eLfRfbjVXDLKSvez6v1BIIbfE6Sst2GKvuxEl8-iggpC1F-qNwNo57tQxOzoktVLTgmVgjNZqPk_qHJaGJ0NHjpX8kcFH54UbMAMeZPCMGUXfDoGD2uxMaQUoXucECO9d5cu7to3LPXeXYV_93Qtj_SDnegfN-zKXw</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Lindquist, David</creator><creator>Alsina, Fernando C</creator><creator>Herdenberg, Carl</creator><creator>Larsson, Catharina</creator><creator>Höppener, Jo</creator><creator>Wang, Na</creator><creator>Paratcha, Gustavo</creator><creator>Tarján, Miklós</creator><creator>Tot, Tibor</creator><creator>Henriksson, Roger</creator><creator>Hedman, Håkan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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genetics</topic><topic>Carcinoma, Neuroendocrine - metabolism</topic><topic>Carcinoma, Papillary - genetics</topic><topic>Carcinoma, Papillary - metabolism</topic><topic>Care and treatment</topic><topic>Development and progression</topic><topic>Down-Regulation</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene mutation</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>LRIG1</topic><topic>M918T</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>MEN2A</topic><topic>MEN2B</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Mutation</topic><topic>Oncology</topic><topic>onkologi</topic><topic>Proto-Oncogene Proteins c-ret - genetics</topic><topic>Proto-Oncogene Proteins c-ret - metabolism</topic><topic>RET</topic><topic>Rodents</topic><topic>Studies</topic><topic>Thyroid cancer</topic><topic>Thyroid Neoplasms - genetics</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Tumor suppressor genes</topic><toplevel>online_resources</toplevel><creatorcontrib>Lindquist, David</creatorcontrib><creatorcontrib>Alsina, Fernando C</creatorcontrib><creatorcontrib>Herdenberg, Carl</creatorcontrib><creatorcontrib>Larsson, Catharina</creatorcontrib><creatorcontrib>Höppener, Jo</creatorcontrib><creatorcontrib>Wang, Na</creatorcontrib><creatorcontrib>Paratcha, Gustavo</creatorcontrib><creatorcontrib>Tarján, Miklós</creatorcontrib><creatorcontrib>Tot, Tibor</creatorcontrib><creatorcontrib>Henriksson, Roger</creatorcontrib><creatorcontrib>Hedman, Håkan</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>Nursing & Allied Health Database</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>PubMed Central (Full Participant titles)</collection><collection>SWEPUB Umeå universitet full text</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Umeå universitet</collection><collection>SwePub Articles full text</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lindquist, David</au><au>Alsina, Fernando C</au><au>Herdenberg, Carl</au><au>Larsson, Catharina</au><au>Höppener, Jo</au><au>Wang, Na</au><au>Paratcha, Gustavo</au><au>Tarján, Miklós</au><au>Tot, Tibor</au><au>Henriksson, Roger</au><au>Hedman, Håkan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LRIG1 negatively regulates RET mutants and is downregulated in thyroid cancer</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>52</volume><issue>4</issue><spage>1189</spage><epage>1197</epage><pages>1189-1197</pages><issn>1019-6439</issn><issn>1791-2423</issn><eissn>1791-2423</eissn><abstract>Papillary thyroid carcinoma (PTC) and medullary thyroid carcinoma (MTC) are characterized by genomic rearrangements and point mutations in the proto-oncogene RET. Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1 expression levels are associated with patient survival in many cancer types. In the present study, we investigated whether the oncogenic RET mutants RET2A (C634R) and RET2B (M918T) were regulated by LRIG1, and the possible effects of LRIG1 expression in thyroid cancer were investigated in three different clinical cohorts and in a RET2B-driven mouse model of MTC. LRIG1 was shown to physically interact with both RET2A and RET2B and to restrict their ligand-independent activation. LRIG1 mRNA levels were downregulated in PTC and MTC compared to normal thyroid gland tissue. There was no apparent association between LRIG1 RNA or protein expression levels and patient survival in the studied cohorts. The transgenic RET2B mice developed pre-cancerous medullary thyroid lesions at a high frequency (36%); however, no overt cancers were observed. There was no significant difference in the incidence of pre-cancerous lesions between Lrig1 wild-type and Lrig1-deficient RET2B mice. In conclusion, the findings that LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in PTC and MTC may suggest that LRIG1 functions as a thyroid tumor suppressor.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29436694</pmid><doi>10.3892/ijo.2018.4273</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2018-04, Vol.52 (4), p.1189-1197 |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; SWEPUB Freely available online |
| subjects | Analysis Animals C634R Carcinoma, Neuroendocrine - genetics Carcinoma, Neuroendocrine - metabolism Carcinoma, Papillary - genetics Carcinoma, Papillary - metabolism Care and treatment Development and progression Down-Regulation Gene expression Gene Expression Regulation, Neoplastic - genetics Gene mutation Genetic aspects Health aspects Humans LRIG1 M918T Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism MEN2A MEN2B Mice Mice, Inbred C57BL Mice, Transgenic Mutation Oncology onkologi Proto-Oncogene Proteins c-ret - genetics Proto-Oncogene Proteins c-ret - metabolism RET Rodents Studies Thyroid cancer Thyroid Neoplasms - genetics Thyroid Neoplasms - metabolism Tumor suppressor genes |
| title | LRIG1 negatively regulates RET mutants and is downregulated in thyroid cancer |
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