LAT-1 and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors
Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analy...
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| Veröffentlicht in: | Cancers 2020-10, Vol.12 (10), p.2968 |
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| creator | Sampedro-Núñez, Miguel Bouthelier, Antonio Serrano-Somavilla, Ana Martínez-Hernández, Rebeca Adrados, Magdalena Martín-Pérez, Elena Muñoz de Nova, José Luis Cameselle-Teijeiro, José Manuel Blanco-Carrera, Concepción Cabezas-Agricola, José Manuel Díaz, José Ángel García-Centeno, Rogelio Aragones, Julian Marazuela, Mónica |
| description | Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors. |
| doi_str_mv | 10.3390/cancers12102968 |
| format | Article |
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We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers12102968</identifier><identifier>PMID: 33066332</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Amino acids ; Angiogenesis ; Breast cancer ; Cell growth ; Cell proliferation ; Gastrointestinal cancer ; Gene expression ; Genetic aspects ; Glucose ; Glucose transporter ; Health aspects ; Hypoxia ; Hypoxia-inducible factors ; Immunohistochemistry ; Malignancy ; Medical prognosis ; Metabolism ; Metastases ; Metastasis ; Mutation ; Neuroendocrine tumors ; Nutrient uptake ; Nutrients ; Oxygen ; Pancreas ; Prognosis ; VHL protein</subject><ispartof>Cancers, 2020-10, Vol.12 (10), p.2968</ispartof><rights>COPYRIGHT 2020 MDPI AG</rights><rights>2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-e1de1cdd1f9f5a628ac8fc485bc8ef789a8cfdb425588dd52e639b5313b6014e3</citedby><cites>FETCH-LOGICAL-c492t-e1de1cdd1f9f5a628ac8fc485bc8ef789a8cfdb425588dd52e639b5313b6014e3</cites><orcidid>0000-0003-1439-5632 ; 0000-0003-2479-1882 ; 0000-0002-5516-8914 ; 0000-0003-1158-9618 ; 0000-0001-8137-5637</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/PMC7602091/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7602091/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Sampedro-Núñez, Miguel</creatorcontrib><creatorcontrib>Bouthelier, Antonio</creatorcontrib><creatorcontrib>Serrano-Somavilla, Ana</creatorcontrib><creatorcontrib>Martínez-Hernández, Rebeca</creatorcontrib><creatorcontrib>Adrados, Magdalena</creatorcontrib><creatorcontrib>Martín-Pérez, Elena</creatorcontrib><creatorcontrib>Muñoz de Nova, José Luis</creatorcontrib><creatorcontrib>Cameselle-Teijeiro, José Manuel</creatorcontrib><creatorcontrib>Blanco-Carrera, Concepción</creatorcontrib><creatorcontrib>Cabezas-Agricola, José Manuel</creatorcontrib><creatorcontrib>Díaz, José Ángel</creatorcontrib><creatorcontrib>García-Centeno, Rogelio</creatorcontrib><creatorcontrib>Aragones, Julian</creatorcontrib><creatorcontrib>Marazuela, Mónica</creatorcontrib><title>LAT-1 and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors</title><title>Cancers</title><description>Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors.</description><subject>Amino acids</subject><subject>Angiogenesis</subject><subject>Breast cancer</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Gastrointestinal cancer</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Glucose transporter</subject><subject>Health aspects</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factors</subject><subject>Immunohistochemistry</subject><subject>Malignancy</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mutation</subject><subject>Neuroendocrine tumors</subject><subject>Nutrient uptake</subject><subject>Nutrients</subject><subject>Oxygen</subject><subject>Pancreas</subject><subject>Prognosis</subject><subject>VHL 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and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors</title><author>Sampedro-Núñez, Miguel ; Bouthelier, Antonio ; Serrano-Somavilla, Ana ; Martínez-Hernández, Rebeca ; Adrados, Magdalena ; Martín-Pérez, Elena ; Muñoz de Nova, José Luis ; Cameselle-Teijeiro, José Manuel ; Blanco-Carrera, Concepción ; Cabezas-Agricola, José Manuel ; Díaz, José Ángel ; García-Centeno, Rogelio ; Aragones, Julian ; Marazuela, Mónica</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-e1de1cdd1f9f5a628ac8fc485bc8ef789a8cfdb425588dd52e639b5313b6014e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Amino acids</topic><topic>Angiogenesis</topic><topic>Breast cancer</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Gastrointestinal cancer</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Glucose transporter</topic><topic>Health aspects</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factors</topic><topic>Immunohistochemistry</topic><topic>Malignancy</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Neuroendocrine tumors</topic><topic>Nutrient uptake</topic><topic>Nutrients</topic><topic>Oxygen</topic><topic>Pancreas</topic><topic>Prognosis</topic><topic>VHL protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sampedro-Núñez, Miguel</creatorcontrib><creatorcontrib>Bouthelier, Antonio</creatorcontrib><creatorcontrib>Serrano-Somavilla, Ana</creatorcontrib><creatorcontrib>Martínez-Hernández, Rebeca</creatorcontrib><creatorcontrib>Adrados, Magdalena</creatorcontrib><creatorcontrib>Martín-Pérez, Elena</creatorcontrib><creatorcontrib>Muñoz de Nova, José 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Tumors</atitle><jtitle>Cancers</jtitle><date>2020-10-13</date><risdate>2020</risdate><volume>12</volume><issue>10</issue><spage>2968</spage><pages>2968-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Cancer cells develop mechanisms that increase nutrient uptake, including key nutrient carriers, such as amino acid transporter 1 (LAT-1) and glucose transporter 1 (GLUT-1), regulated by the oxygen-sensing Von Hippel Lindau-hypoxia-inducible factor (VHL-HIF) transcriptional pathway. We aimed to analyze these metabolic players in gastroenteropancreatic neuroendocrine tumors (GEP-NET) and correlate them with tumor malignancy and progression. LAT-1, GLUT-1, and pVHL expression was analyzed in 116 GEP-NETs and 48 peritumoral tissue samples by immunohistochemistry. LAT-1 was stably silenced using specific shRNA in the human NET BON cell line. LAT-1 expression was significantly increased in tumor tissue compared to non-tumor tissue in both gastrointestinal (67% vs. 44%) and pancreatic NETs (54% vs. 31%). Similarly, GLUT-1 was substantially elevated in gastrointestinal (74% vs. 19%) and pancreatic (58% vs. 4%) NETs. In contrast, pVHL expression was decreased (85% vs. 58%) in pancreatic NETs. Tumors with metastases at diagnosis displayed increased LAT-1 and GLUT-1 and decreased pVHL expression (p < 0.001). In accordance with these data, silencing LAT-1 curtailed cell proliferation in BON cells. These findings suggest that specific mechanisms that increase nutrient uptake, such as LAT-1 and GLUT-1, are increased in GEP-NETs, whereas pVHL is decreased. These markers might be related to the proliferation and metastatic capacity of these tumors.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>33066332</pmid><doi>10.3390/cancers12102968</doi><orcidid>https://orcid.org/0000-0003-1439-5632</orcidid><orcidid>https://orcid.org/0000-0003-2479-1882</orcidid><orcidid>https://orcid.org/0000-0002-5516-8914</orcidid><orcidid>https://orcid.org/0000-0003-1158-9618</orcidid><orcidid>https://orcid.org/0000-0001-8137-5637</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Amino acids Angiogenesis Breast cancer Cell growth Cell proliferation Gastrointestinal cancer Gene expression Genetic aspects Glucose Glucose transporter Health aspects Hypoxia Hypoxia-inducible factors Immunohistochemistry Malignancy Medical prognosis Metabolism Metastases Metastasis Mutation Neuroendocrine tumors Nutrient uptake Nutrients Oxygen Pancreas Prognosis VHL protein |
| title | LAT-1 and GLUT-1 Carrier Expression and Its Prognostic Value in Gastroenteropancreatic Neuroendocrine Tumors |
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