Coupling of glucose deprivation with impaired histone H2B monoubiquitination in tumors
Metabolic reprogramming is associated with tumorigenesis. However, glucose metabolism in tumors is poorly understood. Here, we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins. We show that mono-ubiquitinated histone H...
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| description | Metabolic reprogramming is associated with tumorigenesis. However, glucose metabolism in tumors is poorly understood. Here, we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins. We show that mono-ubiquitinated histone H2B (uH2B) is a semi-quantitative histone marker for glucose. We further show that loss of uH2B occurs specifically in cancer cells from a wide array of tumor specimens of breast, colon, lung and additional 23 anatomic sites. In contrast, uH2B levels remain high in stromal tissues or non-cancerous cells in the tumor specimens. Taken together, our data suggest that glucose deficiency and loss of uH2B are novel properties of cancer cells in vivo, which may represent important regulatory mechanisms of tumorigenesis. |
| doi_str_mv | 10.1371/journal.pone.0036775 |
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Taken together, our data suggest that glucose deficiency and loss of uH2B are novel properties of cancer cells in vivo, which may represent important regulatory mechanisms of tumorigenesis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0036775</identifier><identifier>PMID: 22615809</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biology ; Bioluminescence ; Breast cancer ; Cancer ; Cancer therapies ; Cell cycle ; Cell Line, Tumor ; Colon ; Deprivation ; Glucose ; Glucose - metabolism ; Histone H2B ; Histones - metabolism ; Humans ; Immunohistochemistry ; Lungs ; Medicine ; Metabolism ; Metabolites ; Mutation ; Neoplasms - metabolism ; Physiological aspects ; Proteins ; Regulatory mechanisms (biology) ; Senescence ; Tissues ; Tumorigenesis ; Tumors ; Ubiquitination ; Yeast</subject><ispartof>PloS one, 2012-05, Vol.7 (5), p.e36775-e36775</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Urasaki et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://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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However, glucose metabolism in tumors is poorly understood. Here, we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins. We show that mono-ubiquitinated histone H2B (uH2B) is a semi-quantitative histone marker for glucose. We further show that loss of uH2B occurs specifically in cancer cells from a wide array of tumor specimens of breast, colon, lung and additional 23 anatomic sites. In contrast, uH2B levels remain high in stromal tissues or non-cancerous cells in the tumor specimens. Taken together, our data suggest that glucose deficiency and loss of uH2B are novel properties of cancer cells in vivo, which may represent important regulatory mechanisms of tumorigenesis.</description><subject>Biology</subject><subject>Bioluminescence</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Colon</subject><subject>Deprivation</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Histone H2B</subject><subject>Histones - metabolism</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Lungs</subject><subject>Medicine</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mutation</subject><subject>Neoplasms - metabolism</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Regulatory mechanisms (biology)</subject><subject>Senescence</subject><subject>Tissues</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><subject>Ubiquitination</subject><subject>Yeast</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl1rFDEUhgdRbK3-A9EBQfRi13xnclOoi9qFQsGP3oYkk5lNmZlsJ0nVf2_WnZYd6YXkIuHkOe_JOXmL4iUES4g5_HDt0ziobrn1g10CgBnn9FFxDAVGC4YAfnxwPiqehXANAMUVY0-LI4QYpBUQx8XVyqdt54a29E3Zdsn4YMvabkd3q6LzQ_nTxU3p-q1yo63LjQsx1yvP0cey94NP2t0kF92wh91QxtT7MTwvnjSqC_bFtJ8UPz5_-r46X1xcflmvzi4WhgkUF5XRGgNhKqhVpSkiiBFb1bQmxGhLELRGYIUgZA1vKGc1VgDWCgpijRKVxifF673utvNBTiMJEmJEKOWU40ys90Tt1bXMffVq_C29cvJvwI-tVGN0prMSU1Mx3dQNoppAizUUSEBCFMTUCm6y1ulULene1sYOcVTdTHR-M7iNbP2txJhiQWgWeDcJjP4m2RBl74KxXacG61N-N4CUMC4oyOibf9CHu5uoVuUG3ND4XNfsROUZ4RxwjrDI1PIBKq_a9s7k_2xcjs8S3s8SMhPtr9iqFIJcf_v6_-zl1Zx9e8BurOriJvgu7cwT5iDZg2b0IYy2uR8yBHJn_7tpyJ395WT_nPbq8IPuk-78jv8AnrwAKQ</recordid><startdate>20120516</startdate><enddate>20120516</enddate><creator>Urasaki, Yasuyo</creator><creator>Heath, Linda</creator><creator>Xu, C Wilson</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>PIMPY</scope><scope>PQEST</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></search><sort><creationdate>20120516</creationdate><title>Coupling of glucose deprivation with impaired histone H2B monoubiquitination in tumors</title><author>Urasaki, Yasuyo ; Heath, Linda ; Xu, C Wilson</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-8cbb309c81ba8b524264e8d5d44cbe421ec93a2116f7f576d3a01da194eca98b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Biology</topic><topic>Bioluminescence</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Colon</topic><topic>Deprivation</topic><topic>Glucose</topic><topic>Glucose - 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However, glucose metabolism in tumors is poorly understood. Here, we report that glucose levels are significantly lower in bulk tumor specimens than those in normal tissues of the same tissue origins. We show that mono-ubiquitinated histone H2B (uH2B) is a semi-quantitative histone marker for glucose. We further show that loss of uH2B occurs specifically in cancer cells from a wide array of tumor specimens of breast, colon, lung and additional 23 anatomic sites. In contrast, uH2B levels remain high in stromal tissues or non-cancerous cells in the tumor specimens. Taken together, our data suggest that glucose deficiency and loss of uH2B are novel properties of cancer cells in vivo, which may represent important regulatory mechanisms of tumorigenesis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22615809</pmid><doi>10.1371/journal.pone.0036775</doi><tpages>e36775</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biology Bioluminescence Breast cancer Cancer Cancer therapies Cell cycle Cell Line, Tumor Colon Deprivation Glucose Glucose - metabolism Histone H2B Histones - metabolism Humans Immunohistochemistry Lungs Medicine Metabolism Metabolites Mutation Neoplasms - metabolism Physiological aspects Proteins Regulatory mechanisms (biology) Senescence Tissues Tumorigenesis Tumors Ubiquitination Yeast |
| title | Coupling of glucose deprivation with impaired histone H2B monoubiquitination in tumors |
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