Restoration of type 1 iodothyronine deiodinase expression in renal cancer cells downregulates oncoproteins and affects key metabolic pathways as well as anti-oxidative system
Type 1 iodothyronine deiodinase (DIO1) contributes to deiodination of 3,5,3',5'-tetraiodo-L-thyronine (thyroxine, T4) yielding of 3,5,3'-triiodothyronine (T3), a powerful regulator of cell differentiation, proliferation, and metabolism. Our previous work showed that loss of DIO1 enhan...
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| Veröffentlicht in: | PloS one 2017-12, Vol.12 (12), p.e0190179-e0190179 |
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| creator | Popławski, Piotr Wiśniewski, Jacek R Rijntjes, Eddy Richards, Keith Rybicka, Beata Köhrle, Josef Piekiełko-Witkowska, Agnieszka |
| description | Type 1 iodothyronine deiodinase (DIO1) contributes to deiodination of 3,5,3',5'-tetraiodo-L-thyronine (thyroxine, T4) yielding of 3,5,3'-triiodothyronine (T3), a powerful regulator of cell differentiation, proliferation, and metabolism. Our previous work showed that loss of DIO1 enhances proliferation and migration of renal cancer cells. However, the global effects of DIO1 expression in various tissues affected by cancer remain unknown. Here, the effects of stable DIO1 re-expression were analyzed on the proteome of renal cancer cells, followed by quantitative real-time PCR validation in two renal cancer-derived cell lines. DIO1-induced changes in intracellular concentrations of thyroid hormones were quantified by L-MS/MS and correlations between expression of DIO1 and potential target genes were determined in tissue samples from renal cancer patients. Stable re-expression of DIO1, resulted in 26 downregulated proteins while 59 proteins were overexpressed in renal cancer cells. The 'downregulated' group consisted mainly of oncoproteins (e.g. STAT3, ANPEP, TGFBI, TGM2) that promote proliferation, migration and invasion. Furthermore, DIO1 re-expression enhanced concentrations of two subunits of thyroid hormone transporter (SLC7A5, SLC3A2), enzymes of key pathways of cellular energy metabolism (e.g. TKT, NAMPT, IDH2), sex steroid metabolism and anti-oxidative response (AKR1C2, AKR1B10). DIO1 expression resulted in elevated intracellular concentration of T4. Expression of DIO1-affected genes strongly correlated with DIO1 transcript levels in tissue samples from renal cancer patients as well as with their poor survival. This first study addressing effects of deiodinase re-expression on proteome of cancer cells demonstrates that induced DIO1 re-expression in renal cancer robustly downregulates oncoproteins, affects key metabolic pathways, and triggers proteins involved in anti-oxidative protection. This data supports the notion that suppressed DIO1 expression and changes in local availability of thyroid hormones might favor a shift from a differentiated to a more proliferation-prone state of cancer tissues and cell lines. |
| doi_str_mv | 10.1371/journal.pone.0190179 |
| format | Article |
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Our previous work showed that loss of DIO1 enhances proliferation and migration of renal cancer cells. However, the global effects of DIO1 expression in various tissues affected by cancer remain unknown. Here, the effects of stable DIO1 re-expression were analyzed on the proteome of renal cancer cells, followed by quantitative real-time PCR validation in two renal cancer-derived cell lines. DIO1-induced changes in intracellular concentrations of thyroid hormones were quantified by L-MS/MS and correlations between expression of DIO1 and potential target genes were determined in tissue samples from renal cancer patients. Stable re-expression of DIO1, resulted in 26 downregulated proteins while 59 proteins were overexpressed in renal cancer cells. The 'downregulated' group consisted mainly of oncoproteins (e.g. STAT3, ANPEP, TGFBI, TGM2) that promote proliferation, migration and invasion. Furthermore, DIO1 re-expression enhanced concentrations of two subunits of thyroid hormone transporter (SLC7A5, SLC3A2), enzymes of key pathways of cellular energy metabolism (e.g. TKT, NAMPT, IDH2), sex steroid metabolism and anti-oxidative response (AKR1C2, AKR1B10). DIO1 expression resulted in elevated intracellular concentration of T4. Expression of DIO1-affected genes strongly correlated with DIO1 transcript levels in tissue samples from renal cancer patients as well as with their poor survival. This first study addressing effects of deiodinase re-expression on proteome of cancer cells demonstrates that induced DIO1 re-expression in renal cancer robustly downregulates oncoproteins, affects key metabolic pathways, and triggers proteins involved in anti-oxidative protection. This data supports the notion that suppressed DIO1 expression and changes in local availability of thyroid hormones might favor a shift from a differentiated to a more proliferation-prone state of cancer tissues and cell lines.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0190179</identifier><identifier>PMID: 29272308</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Amino acids ; Antioxidants - metabolism ; Apoptosis ; Biochemistry ; Biology and Life Sciences ; Biotechnology ; Cancer ; Cancer cells ; Cell culture ; Cell cycle ; Cell differentiation ; Cell Line, Tumor ; Cell migration ; Cell proliferation ; Colorectal cancer ; Down-Regulation ; Energy metabolism ; Gene expression ; Genes ; Genetic aspects ; Health education ; Homogenization ; Hormones ; Humans ; Intracellular ; Iodide peroxidase ; Iodide Peroxidase - metabolism ; Iodine ; Iodine (Nutrient) ; Kidney cancer ; Kidney Neoplasms - enzymology ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - pathology ; Kidneys ; Medicine and Health Sciences ; Metabolic pathways ; Metabolism ; Metabolites ; Molecular biology ; Oncogene Proteins - metabolism ; Oncoproteins ; Oxidative metabolism ; Patients ; Physiological aspects ; Proteins ; Proteomes ; Proteomics ; Real-Time Polymerase Chain Reaction ; Renal cell carcinoma ; Research and Analysis Methods ; Restoration ; Stat3 protein ; Thyroid ; Thyroid gland ; Thyroid hormones ; Thyroxine ; Thyroxine - metabolism ; Thyroxine deiodinase ; Tissues ; Transcription ; Triiodothyronine ; Tumor cell lines ; Tumors</subject><ispartof>PloS one, 2017-12, Vol.12 (12), p.e0190179-e0190179</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Popławski et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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Our previous work showed that loss of DIO1 enhances proliferation and migration of renal cancer cells. However, the global effects of DIO1 expression in various tissues affected by cancer remain unknown. Here, the effects of stable DIO1 re-expression were analyzed on the proteome of renal cancer cells, followed by quantitative real-time PCR validation in two renal cancer-derived cell lines. DIO1-induced changes in intracellular concentrations of thyroid hormones were quantified by L-MS/MS and correlations between expression of DIO1 and potential target genes were determined in tissue samples from renal cancer patients. Stable re-expression of DIO1, resulted in 26 downregulated proteins while 59 proteins were overexpressed in renal cancer cells. The 'downregulated' group consisted mainly of oncoproteins (e.g. STAT3, ANPEP, TGFBI, TGM2) that promote proliferation, migration and invasion. Furthermore, DIO1 re-expression enhanced concentrations of two subunits of thyroid hormone transporter (SLC7A5, SLC3A2), enzymes of key pathways of cellular energy metabolism (e.g. TKT, NAMPT, IDH2), sex steroid metabolism and anti-oxidative response (AKR1C2, AKR1B10). DIO1 expression resulted in elevated intracellular concentration of T4. Expression of DIO1-affected genes strongly correlated with DIO1 transcript levels in tissue samples from renal cancer patients as well as with their poor survival. This first study addressing effects of deiodinase re-expression on proteome of cancer cells demonstrates that induced DIO1 re-expression in renal cancer robustly downregulates oncoproteins, affects key metabolic pathways, and triggers proteins involved in anti-oxidative protection. This data supports the notion that suppressed DIO1 expression and changes in local availability of thyroid hormones might favor a shift from a differentiated to a more proliferation-prone state of cancer tissues and cell lines.</description><subject>Amino acids</subject><subject>Antioxidants - metabolism</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell differentiation</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Colorectal cancer</subject><subject>Down-Regulation</subject><subject>Energy metabolism</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health education</subject><subject>Homogenization</subject><subject>Hormones</subject><subject>Humans</subject><subject>Intracellular</subject><subject>Iodide peroxidase</subject><subject>Iodide Peroxidase - metabolism</subject><subject>Iodine</subject><subject>Iodine (Nutrient)</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - enzymology</subject><subject>Kidney Neoplasms - metabolism</subject><subject>Kidney Neoplasms - pathology</subject><subject>Kidneys</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic pathways</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Molecular biology</subject><subject>Oncogene Proteins - metabolism</subject><subject>Oncoproteins</subject><subject>Oxidative metabolism</subject><subject>Patients</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Proteomes</subject><subject>Proteomics</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Renal cell carcinoma</subject><subject>Research and Analysis Methods</subject><subject>Restoration</subject><subject>Stat3 protein</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid hormones</subject><subject>Thyroxine</subject><subject>Thyroxine - metabolism</subject><subject>Thyroxine deiodinase</subject><subject>Tissues</subject><subject>Transcription</subject><subject>Triiodothyronine</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk8tu1DAUhiMEoqXwBggsISFYTLGd2Ik3SFXFZaRKlcplaznO8YxLxg620868FM-IQ9Oqg1iw8uV8_s_NpyieE3xMypq8u_RjcKo_HryDY0wEJrV4UBwSUdIFp7h8eG9_UDyJ8RJjVjacPy4OqKA1LXFzWPy6gJh8UMl6h7xBaTcAIsj6zqf1LnhnHaAO8tk6FQHBdggQ40RbhwLkCJBWTkNAGvo-os5fuwCrsVcJIvJO-yH4BNZFpFyHlDGgU0Q_YIc2kFTre6vRoNL6Wu0yEtF1lplW5ZJd-K3tcmxXgOIuJtg8LR4Z1Ud4Nq9HxbePH76efl6cnX9anp6cLTRryrRgUJm2pEBbqFvdGa5MyzEWnDUNJxiTbOfEaMyBCg5doxtTc8yMokaJmpRHxcsb3aH3Uc6ljpKIWghGhKgzsbwhOq8u5RDsRoWd9MrKPxc-rKQKyeoeJDGsZo2hvKKiEi1rBBcsx6F1xXVbi6z1fvY2thvoNLgUVL8num9xdi1X_kqyuiK0arLAm1kg-J9j7qjc2Dj1Qznw4xx3jRmhGX31F_rv7GZqpXIC1hmf_epJVJ4wivNPwmKq0ts9SnuXYJtWaoxRLr9c_D97_n2ffX2PXYPq0zr6fpw-adwHqxtQBx9jAHNXM4LlNCW3yclpSuQ8JfnZi_v1vnt0Oxblbx6SEWY</recordid><startdate>20171222</startdate><enddate>20171222</enddate><creator>Popławski, Piotr</creator><creator>Wiśniewski, Jacek R</creator><creator>Rijntjes, Eddy</creator><creator>Richards, Keith</creator><creator>Rybicka, Beata</creator><creator>Köhrle, Josef</creator><creator>Piekiełko-Witkowska, Agnieszka</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5348-0760</orcidid></search><sort><creationdate>20171222</creationdate><title>Restoration of type 1 iodothyronine deiodinase expression in renal cancer cells downregulates oncoproteins and affects key metabolic pathways as well as anti-oxidative system</title><author>Popławski, Piotr ; Wiśniewski, Jacek R ; Rijntjes, Eddy ; Richards, Keith ; Rybicka, Beata ; Köhrle, Josef ; Piekiełko-Witkowska, Agnieszka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c583t-5e4fb32e2be7bcdf6afb6009658861001e4f61fc06e296ed8c8f7605fa2fa9713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Amino acids</topic><topic>Antioxidants - 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metabolism</topic><topic>Oncoproteins</topic><topic>Oxidative metabolism</topic><topic>Patients</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Proteomes</topic><topic>Proteomics</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Renal cell carcinoma</topic><topic>Research and Analysis Methods</topic><topic>Restoration</topic><topic>Stat3 protein</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid hormones</topic><topic>Thyroxine</topic><topic>Thyroxine - metabolism</topic><topic>Thyroxine deiodinase</topic><topic>Tissues</topic><topic>Transcription</topic><topic>Triiodothyronine</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Popławski, Piotr</creatorcontrib><creatorcontrib>Wiśniewski, Jacek R</creatorcontrib><creatorcontrib>Rijntjes, Eddy</creatorcontrib><creatorcontrib>Richards, Keith</creatorcontrib><creatorcontrib>Rybicka, Beata</creatorcontrib><creatorcontrib>Köhrle, Josef</creatorcontrib><creatorcontrib>Piekiełko-Witkowska, Agnieszka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Popławski, Piotr</au><au>Wiśniewski, Jacek R</au><au>Rijntjes, Eddy</au><au>Richards, Keith</au><au>Rybicka, Beata</au><au>Köhrle, Josef</au><au>Piekiełko-Witkowska, Agnieszka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Restoration of type 1 iodothyronine deiodinase expression in renal cancer cells downregulates oncoproteins and affects key metabolic pathways as well as anti-oxidative system</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-12-22</date><risdate>2017</risdate><volume>12</volume><issue>12</issue><spage>e0190179</spage><epage>e0190179</epage><pages>e0190179-e0190179</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Type 1 iodothyronine deiodinase (DIO1) contributes to deiodination of 3,5,3',5'-tetraiodo-L-thyronine (thyroxine, T4) yielding of 3,5,3'-triiodothyronine (T3), a powerful regulator of cell differentiation, proliferation, and metabolism. Our previous work showed that loss of DIO1 enhances proliferation and migration of renal cancer cells. However, the global effects of DIO1 expression in various tissues affected by cancer remain unknown. Here, the effects of stable DIO1 re-expression were analyzed on the proteome of renal cancer cells, followed by quantitative real-time PCR validation in two renal cancer-derived cell lines. DIO1-induced changes in intracellular concentrations of thyroid hormones were quantified by L-MS/MS and correlations between expression of DIO1 and potential target genes were determined in tissue samples from renal cancer patients. Stable re-expression of DIO1, resulted in 26 downregulated proteins while 59 proteins were overexpressed in renal cancer cells. The 'downregulated' group consisted mainly of oncoproteins (e.g. STAT3, ANPEP, TGFBI, TGM2) that promote proliferation, migration and invasion. Furthermore, DIO1 re-expression enhanced concentrations of two subunits of thyroid hormone transporter (SLC7A5, SLC3A2), enzymes of key pathways of cellular energy metabolism (e.g. TKT, NAMPT, IDH2), sex steroid metabolism and anti-oxidative response (AKR1C2, AKR1B10). DIO1 expression resulted in elevated intracellular concentration of T4. Expression of DIO1-affected genes strongly correlated with DIO1 transcript levels in tissue samples from renal cancer patients as well as with their poor survival. This first study addressing effects of deiodinase re-expression on proteome of cancer cells demonstrates that induced DIO1 re-expression in renal cancer robustly downregulates oncoproteins, affects key metabolic pathways, and triggers proteins involved in anti-oxidative protection. This data supports the notion that suppressed DIO1 expression and changes in local availability of thyroid hormones might favor a shift from a differentiated to a more proliferation-prone state of cancer tissues and cell lines.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>29272308</pmid><doi>10.1371/journal.pone.0190179</doi><tpages>e0190179</tpages><orcidid>https://orcid.org/0000-0002-5348-0760</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-12, Vol.12 (12), p.e0190179-e0190179 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1979951997 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Amino acids Antioxidants - metabolism Apoptosis Biochemistry Biology and Life Sciences Biotechnology Cancer Cancer cells Cell culture Cell cycle Cell differentiation Cell Line, Tumor Cell migration Cell proliferation Colorectal cancer Down-Regulation Energy metabolism Gene expression Genes Genetic aspects Health education Homogenization Hormones Humans Intracellular Iodide peroxidase Iodide Peroxidase - metabolism Iodine Iodine (Nutrient) Kidney cancer Kidney Neoplasms - enzymology Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Kidneys Medicine and Health Sciences Metabolic pathways Metabolism Metabolites Molecular biology Oncogene Proteins - metabolism Oncoproteins Oxidative metabolism Patients Physiological aspects Proteins Proteomes Proteomics Real-Time Polymerase Chain Reaction Renal cell carcinoma Research and Analysis Methods Restoration Stat3 protein Thyroid Thyroid gland Thyroid hormones Thyroxine Thyroxine - metabolism Thyroxine deiodinase Tissues Transcription Triiodothyronine Tumor cell lines Tumors |
| title | Restoration of type 1 iodothyronine deiodinase expression in renal cancer cells downregulates oncoproteins and affects key metabolic pathways as well as anti-oxidative system |
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