Nicol, Christopher J B - Queen's University - Department of Biomedical and Molecular Sciences

个人简介

Research in my laboratory is focused on the cell-specific roles of the peroxisome proliferator-activated receptors (PPARs), of which there are three family members (alpha, delta/beta and gamma), with respect to cancer.ÊCurrently, our goal is to gain a thorough understanding of the processes involved in breast cancer at the genetic, cellular and whole body levels. The laboratory is using state-of-the-art methods to complement in vivo PPAR knockout mouse studies with in vitro and molecular techniques. Ultimately, we aim to develop innovative strategies for identifying those individuals at increased risk for breast cancer, improve the effectiveness of the therapeutic approaches used, and hopefully prevent this disease in susceptible populations.

研究领域

Research in my laboratory is focused on the cell-specific roles of the peroxisome proliferator-activated receptors (PPARs), of which there are three family members (alpha, delta/beta and gamma), with respect to cancer. PPARs are ligand-activated transcription factors, belonging to the nuclear receptor superfamily, that regulate expression of downstream target genes containing specific promoter recognition sequences known as peroxisome proliferator responsive elements (PPREs). PPARs are themselves expressed in a number of cell/tissue types. For example, PPARg expression has been identified in adipocytes (fat cells), and cells of the breast, liver, colon, prostate, and cardiovascular and immune systems. Several synthetic compounds used to successfully treat various human disorders for many years, and now identified as PPAR ligands, helped establish critical regulatory roles for PPARs in lipid and glucose metabolism. Interestingly, in vitro and in vivo studies since the late 1990s have suggested the PPARs may play important roles in carcinogenesis. However, the molecular mechanisms linking PPARs to the regulation of cell growth and transformation are only partially understood. Currently, our goal is to gain a thorough understanding of the processes involved in breast cancer at the genetic, cellular and whole body levels. The laboratory is using state-of-the-art methods to complement in vivo PPAR knockout mouse studies with in vitro and molecular techniques. Ultimately, we aim to develop innovative strategies for identifying those individuals at increased risk for breast cancer, improve the effectiveness of the therapeutic approaches used, and hopefully prevent this disease in susceptible populations.

近期论文

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W. Shan, C.J. Nicol, S. Ito, M.T. Bility, M.J. Kennett, J.M. Ward, F.J. Gonzalez and J.M. Peters (2008). Peroxisome proliferator-activated receptor-b/d protects against chemically-induced liver toxicity in mice. Hepatology 47: 225-235. M.B. Crosby, J. Zhang, T.M. Nowling, J.L. Svenson, C.J. Nicol, F.J. Gonzalez and G.S. Gilkeson (2006). Inflammatory modulation of PPARg expression and activty. Clin. Immunol. 118: 276-283. C.J. Nicol, M. Adachi, T.E. Akiyama and F.J. Gonzalez (2005). PPARg in endothelial cells influences high fat diet-induced hypertension. Am. J. Hypertens. 18: 549-556. M.B. Crosby, J.L. Svenson, J. Zhang, C.J. Nicol, F.J. Gonzalez and G.S. Gilkeson (2005). Peroxisome proliferation-activated receptor (PPAR)g is not necessary for synthetic PPARg agonist inhibition of inducible nitric-oxide synthase and nitric oxide. J. Pharmacol. Exp. Ther. 312: 69=76. C.J. Nicol, M. Yoon, J.M. Ward, M. Yamashita, K. Fukamachi, J.M. Peters and F.J. Gonzalez (2004). PPARg influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis. Carcinogenesis 25: 1747-1755. F.S. Harman*, C.J. Nicol*, H.E. Marin, J.M. Ward, F.J. Gonzalez and J.M. Peters (2004). Peroxisome proliferators-activated receptor-d attenuates colon carcinogenesis. Nat. Med. 10: 481-483. (*equally contributing co-first authors) T.E. Akiyama*, G. Lambert*, C.J. Nicol*, K. Matsusue, J.M. Peters, H.B. Jr. Brewer and F.J. Gonzalez (2004). Peroxisome proliferators-activated receptor b/d regulates very low density lipoprotein production and catabolism in mice on a Western diet. J. Biol. Chem. 279: 20874-20881. (*equally contributing co-first authors) C. Cheung, T.E. Akiyama, J.M. Ward, C.J. Nicol, L. Feigenbaum, C. Vinson and F.J. Gonzalez (2004). Diminished hepatocellular proliferation in mice humanized for the nuclear receptor peroxisome proliferators-activated receptor a. Cancer Res. 64: 3849-3854. C.J. Nicol, J. Zielenski, L-C. Tsui and P.G. Wells (2000). An embryoprotective role for glucose-6-phosphate dehydrogenase in developmental oxidative stress and chemical teratogenesis. FASEB J. 14: 111-127. C.J. Nicol, M.L. Harrison, R.R. Laposa, I.L. Gimelshtein and P.G. Wells (1995). p53--A teratologic suppressor role for p53 in benzo[a]pyrene treated transgenic p53-deficient mice. Nat. Genet. 10: 181-187.