Journal of Cellular Biochemistry
© Wiley Periodicals, Inc.
Edited By: C. Fred Fox, Gary S. Stein, and Max M. Burger
Impact Factor: 3.263
ISI Journal Citation Reports © Ranking: 2014: 93/184 (Cell Biology); 107/289 (Biochemistry & Molecular Biology)
Online ISSN: 1097-4644
Recently Published Issues
Top Cited Articles 2014
Gillies, L. A. and Kuwana, T.
Apoptosis Regulation at the Mitochondrial Outer Membrane
Journal of Cellular Biochemistry 2014, vol. 115, p. 632
Song, L., Li, Y., Li, W., Wu, S. and Li, Z.
miR-495 Enhances the Sensitivity of Non-Small Cell Lung Cancer Cells to Platinum by Modulation of Copper-Transporting P-type Adenosine Triphosphatase A (ATP7A)
Journal of Cellular Biochemistry 2014, vol. 115, p. 1234
Shang, J., Yang, F., Wang, Y., Wang, Y., Xue, G., Mei, Q., Wang, F. and Sun, S..
MicroRNA-23a Antisense Enhances 5-Fluorouracil Chemosensitivity Through APAF-1/Caspase-9 Apoptotic Pathway in Colorectal Cancer Cells
Journal of Cellular Biochemistry 2014, vol. 115, p. 772
Tsimbouri, P., Gadegaard, N., Burgess, K., White, K., Reynolds, P., Herzyk, P., Oreffo, R. and Dalby, M. J
Nanotopographical Effects on Mesenchymal Stem Cell Morphology and Phenotype
Journal of Cellular Biochemistry 2014, vol. 115, p. 380
Cai, Y., Cai, T. and Chen, Y.
Wnt Pathway in Osteosarcoma, from Oncogenic to Therapeutic
Journal of Cellular Biochemistry 2014, vol. 115, p. 625
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JCB Spotlight Article
Diane M. Jaworski, Aryan M.A. Namboodiri and John R. Moffett
Metabolic networks are significantly altered in neoplastic cells. This altered metabolic program leads to increased glycolysis and lipogenesis and decreased dependence on oxidative phosphorylation and oxygen consumption. Despite their limited mitochondrial respiration, cancer cells, nonetheless, derive sufficient energy from alternative carbon sources and metabolic pathways to maintain cell proliferation. They do so, in part, by utilizing fatty acids, amino acids, ketone bodies and acetate, in addition to glucose. The alternative pathways used in the metabolism of these carbon sources provide opportunities for therapeutic manipulation. Acetate, in particular, has garnered increased attention in the context of cancer as both an epigenetic regulator of posttranslational protein modification, and as a carbon source for cancer cell biomass accumulation. However, to date, the data have not provided a clear understanding of the precise roles that protein acetylation and acetate oxidation play in carcinogenesis, cancer progression or treatment. This review highlights some of the major issues, discrepancies and opportunities associated with the manipulation of acetate metabolism and acetylation-based signaling in cancer development and treatment.