Susan L. Naylor, Ph.D.Professor
University of Texas Medical Branch, 1977
Dr. Naylor has served three terms on NIH study sections as well as reviewed for other agencies and the Army Breast and Prostate Cancers Programs. She is an Associate Editor for Genomics and has served on the editorial board of 4 other journals. Dr. Naylor has been an active member of the American Society of Human Genetics, serving as Chair of the Program Committee and on the Board of Directors. She was on the Program Committee for the 10th International Congress of Human Genetics in Vienna. She has received the Distinguished Alumnus Award from the University of Texas Medical Branch, the Barbara Bowman Award for Contributions to Genetics from the Texas Genetics Society, the Distinguished Service Award from the Texas Genetics Society, and was named the Presidential Distinguished Scholar at UTHSCSA. She co-directs the Genetics and the Molecular Oncology courses in the graduate school. She teaches Bioinformatics in various programs at the Health Science Center. Dr. Naylor received the Presidential Teaching Award in 2008 and in 2009 was named to the University of Texas Academy of Health Science Education. She is currently the chair of the Committee on Graduate Studies for Cellular & Structural Biology and co-leader of the Cancer Biology Track of the IMGP.
We have two projects exploring the role of microRNAs in cancer and in aging. Over 50,000 Americans are diagnosed with kidney cancer and 13,000 die of this disease each year. Despite the prevalence of this cancer, the diagnosis of this disease is often by chance. MicroRNAs play an important role in cancer. One of these small RNA molecules has the potential of regulating several genes. From our studies and others, kidney cancer has a distinct set of miRNAs that are either up- or down-regulated in kidney cancer. Using miRNA microarrays we found that there were 6 known miRNAs that had increased expression in kidney cancer with a greater than 2 fold difference and a t-test p-value <0.001 (miR-34b, miR-122a, miR-210, miR-34a, miR-18b and miR-155). In addition there were 3 predicted miRNAs which also had increased expression. Six known miRNAs had decreased expression in the kidney tumors (miR-200c, miR-187, mir-138, miR-141, miR-188, and miR-509) as well as 15 predicted miRNAs. We are extending these studies to determine whether miRNAs associated with kidney cancer can be detected in biological fluids such as serum or urine. In addition, we are identifying the target genes of these miRNA using bioinformatic analyses.
The second project tests the hypothesis that miRNA expression is modulated in specific tissues during the lifespan of mice. We first examined the expression of miRNAs in liver by microarrays. Several known miRNAs were found to be expressed greater in old mice than in young mice. We verified the expression of miRNAs using realtime RT PCR. The marker that shows the highest difference is miR-155 which is expressed 2.67 times higher in old mice (p = 0.022). This miRNA has been shown to be necessary for normal immune function (Vigorito, 2007). miR-155 and miR-181b which is also expressed higher in old mice are both associated with tumorigenesis. To determine if the changes we observe with age are important in aging, we will measure the miRNA expression in if two anti-aging models (dietary restriction and the Ames dwarf mouse). This study will determine whether the expression of specific miRNAs significantly changes with age and whether genetic or dietary manipulation affects the age-related changes. We hypothesize that specific miRNAs will be associated with aging and that those miRNAs involved in aging will be modulated by either dietary restriction or by dwarfism.
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Muzny DM, Scherer SE, Kaul R, Wang J, Yu J, Sudbrak R, Buhay CJ, Chen R, Cree A, Ding Y, Dugan-Rocha S, Gill R, Gunaratne P, Harris RA, Hawes AC, Hernandez J, Hodgson AV, Hume J, Jackson A, Khan ZM, Kovar-Smith C, Lewis LR, Lozado RJ, Metzker ML, Milosavljevic A, Miner GR, Morgan MB, Nazareth LV, Scott G, Sodergren E, Song XZ, Steffen D, Wei S, Wheeler DA, Wright MW, Worley KC, Yuan Y, Zhang Z, Adams CQ, Ansari-Lari MA, Ayele M, Brown MJ, Chen G, Chen Z, Clendenning J, Clerc-Blankenburg KP, Chen R, Chen Z, Davis C, Delgado O, Dinh HH, Dong W, Draper H, Ernst S, Fu G, Gonzalez-Garay ML, Garcia DK, Gillett W, Gu J, Hao B, Haugen E, Havlak P, He X, Hennig S, Hu S, Huang W, Jackson LR, Jacob LS, Kelly SH, Kube M, Levy R, Li Z, Liu B, Liu J, Liu W, Lu J, Maheshwari M, Nguyen BV, Okwuonu GO, Palmeiri A, Pasternak S, Perez LM, Phelps KA, Plopper FJ, Qiang B, Raymond C, Rodriguez R, Saenphimmachak C, Santibanez J, Shen H, Shen Y, Subramanian S, Tabor PE, Verduzco D, Waldron L, Wang J, Wang J, Wang Q, Williams GA, Wong GK, Yao Z, Zhang J, Zhang X, Zhao G, Zhou J, Zhou Y, Nelson D, Lehrach H, Reinhardt R, Naylor SL, Yang H, Olson M, Weinstock G, Gibbs RA. The DNA sequence, annotation and analysis of human chromosome 3. Nature. 2006 Apr 27;440(7088):1194-8.
Vijayakumar S, Hall DC, Reveles XT, Troyer DA, Thompson IM, Garcia D, Xiang R, Leach RJ, Johnson-Pais TL, Naylor SL. Detection of recurrent copy number loss at Yp11.2 involving TSPY gene cluster in prostate cancer using array-based comparative genomic hybridization. Cancer Res. 2006 Apr 15;66(8):4055-64.
Vijayakumar S, Garcia D, Hensel CH, Banerjee M, Bracht T, Xiang R, Kagan J, Naylor SL. (2005). The human Y chromosome suppresses the tumorigenicity of PC-3, a human prostate cancer cell line, in athymic nude mice. Genes Chromosomes Cancer Dec;44(4):365-72.
Tse C, Xiang RH, Bracht T, Naylor SL. (2002) Human Semaphorin 3B (SEMA3B) located at chromosome 3p21.3 suppresses tumor formation in an adenocarcinoma cell line. Cancer Res. 2002 Jan 15;62(2):542-6.
Xiang R, Davalos AR, Hensel CH, Zhou XJ, Tse C, Naylor SL. (2002). Semaphorin 3F gene from human 3p21.3 suppresses tumor formation in nude mice. Cancer Res. 2002 May 1;62(9):2637-43.