coupling of glucose deprivation with impaired histone h2b monoubiquitination in tumors耦合的葡萄糖剥夺受损组蛋白h2b monoubiquitination肿瘤.pdfVIP

Coupling of Glucose Deprivation with Impaired Histone H2B Monoubiquitination in Tumors 1 1 1,2 Yasuyo Urasaki , Linda Heath , C. Wilson Xu * 1 Nevada Cancer Institute, Las Vegas, Nevada, United States of America, 2 The Biological Research Institute, Pasadena, California, United States of America Abstract 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. Citation: Urasaki Y, Heath L, Xu CW (2012) Coupling of Glucose Deprivation with Impaired Histone H2B Monoubiquitination in Tumors. PLoS ONE 7(5): e36775. doi:10.1371/journal.pone.0036775 Editor: Arthur J. Lustig, Tulane University Health Sciences Center, United States of America Received December 30, 2011; Accepted April 5, 2012; Published May 16, 2012 Copyright: 2012 Urasaki et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Funding: The work is supported by a Department of