1.
Protein-protein interaction network analyses for elucidating the roles of LOXL2-delta72 in esophageal squamous cell carcinoma.
Wu, BL, Zou, HY, Lv, GQ, Du, ZP, Wu, JY, Zhang, PX, Xu, LY, Li, EM
Asian Pacific journal of cancer prevention : APJCP. 2014;(5):2345-51
Abstract
Lysyl oxidase-like 2 (LOXL2), a member of the lysyl oxidase (LOX) family, is a copper-dependent enzyme that catalyzes oxidative deamination of lysine residues on protein substrates. LOXL2 was found to be overexpressed in esophageal squamous cell carcinoma (ESCC) in our previous research. We later identified a LOXL2 splicing variant LOXL2-delta72 and we overexpressed LOXL2-delta72 and its wild type counterpart in ESCC cells following microarray analyses. First, the differentially expressed genes (DEGs) of LOXL2 and LOXL2-delta72 compared to empty plasmid were applied to generate protein-protein interaction (PPI) sub-networks. Comparison of these two sub-networks showed hundreds of different proteins. To reveal the potential specific roles of LOXL2- delta72 compared to its wild type, the DEGs of LOXL2-delta72 vs LOXL2 were also applied to construct a PPI sub-network which was annotated by Gene Ontology. The functional annotation map indicated the third PPI sub-network involved hundreds of GO terms, such as "cell cycle arrest", "G1/S transition of mitotic cell cycle", "interphase", "cell-matrix adhesion" and "cell-substrate adhesion", as well as significant "immunity" related terms, such as "innate immune response", "regulation of defense response" and "Toll signaling pathway". These results provide important clues for experimental identification of the specific biological roles and molecular mechanisms of LOXL2-delta72. This study also provided a work flow to test the different roles of a splicing variant with high-throughput data.
2.
Chemoprevention in gastrointestinal cancers: current status.
Grau, MV, Rees, JR, Baron, JA
Basic & clinical pharmacology & toxicology. 2006;(3):281-7
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Abstract
Chemoprevention, pharmacological intervention for disease prevention, aims to intervene in pathways that lead to clinical disease before the disease occurs. Cancer chemoprevention is a relatively new field, but for gastrointestinal cancers, clinical trials have highlighted the chemopreventive potential of several agents. For colorectal neoplasia, trials with aspirin and other non-steroidal anti-inflammatory drugs (NSAIDS) and calcium have demonstrated the most significant reductions of risk. In observational studies, NSAIDs also consistently appear to protect against oesophageal and gastric cancer. Calcium, and perhaps vitamin D, are also promising and have the advantage of being inexpensive, safe interventions. For the prevention of oesophageal cancer, antitumour-B and retinamide have provided hopeful results, although it is not clear that these findings can be extrapolated from the study populations in Asia to western countries. Evidence from China suggests that a combination of beta-carotene, alpha-tocopherol and selenium may protect against oesophageal cancer, but the relative importance of each agent is unclear, and, again, their effects in other populations has not yet been assessed. Mass immunization against hepatitis B seems to be the most effective means of reducing the incidence of hepatocellular cancer worldwide. In addition, treatment with interferon alpha in patients chronically infected with hepatitis C virus shows considerable promise, given the increasing prevalence of hepatitis C virus carriage in recent years. TJ-9, polyprenoic acid and anti-aflatoxin compounds are also possible avenues that deserve future research.