Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer.

Peroxiredoxins (Prxs), a family of peroxidases, are reactive oxygen species scavengers that hydrolyze H2O2 through catalytic cysteine. Mammalian Prxs comprise six isoforms (typical 2-Cys Prxs; Prx1–4, atypical 2-Cys Prx; Prx5, and 1-Cys Prx; Prx6) that are distributed over various cellular compartments as they are classified according to the position and number of conserved cysteine. 2-Cys Prx1 and Prx2 are abundant proteins that are ubiquitously expressed mainly in the cytosol, and over 90% of their amino acid sequences are homologous. Prx1 and Prx2 protect cells from ROS-mediated oxidative stress through the elimination of H2O2 and regulate cellular signaling through redox-dependent mechanism. In addition, Prx1 and Prx2 are able to bind to a diversity of interaction partners to regulate other various cellular processes in cancer (i.e., regulation of the protein redox status, cell growth, apoptosis, and tumorigenesis). Thus, Prx1 and Prx2 can be potential therapeutic targets and it is particularly important to control their level or activity. This review focuses on cytosolic 2-Cys Prx1 and Prx2 and their role in the regulation of redox signaling based on protein-protein interaction.

Peroxiredoxins (Prxs) are antioxidant enzymes that protect cells from oxidative stress by reducing intracellular accumulation of reactive oxygen species (ROS). In mammalian cells, the six Prx isoforms are ubiquitously expressed in diverse intracellular locations. They are involved in the regulation of various physiological processes including cell growth, differentiation, apoptosis, immune response and metabolism as well as intracellular ROS homeostasis. Although there are increasing evidences that Prxs are involved in carcinogenesis of many cancers, their role in cancer is controversial. The ROS levels in cancer cells are increased compared to normal cells, thus promoting cancer development. Nevertheless, for various cancer types, an overexpression of Prxs has been found to be associated with poor patient prognosis, and an increasing number of studies have reported that tumorigenesis is either facilitated or inhibited by regulation of cancer-associated signaling pathways. This review summarizes Prx isoforms and their basic functions, the relationship between the expression level and the physiological role of Prxs in cancer cells, and their roles in regulating cancer-associated signaling pathways.

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Apios americana Medik tubers are medicinal foods with anti-cancer and anti-inflammatory activities. However, mechanisms of immunostimulatory action of the Apios tuber extract (ATE) on macrophages have not been elucidated. In the present study, we investigated whether ATE could modulate immune responses, such as production of nitric oxide (NO), proinflammatory cytokines, and transcription factors, in RAW264.7 macrophage cells. ATE significantly increased the production of NO and proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), and induced the mRNA and protein levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and proinflammatory cytokines in a dose-dependent manner. Furthermore, Western blot analysis revealed that ATE activated the transcription factor Nuclear Factor-κB and mitogen-activated protein kinases signaling cascades, including extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 kinase. In addition, we found that ATE induced the activation of macrophages through upregulation of toll-like receptor 4 (TLR4) and TLR2. Taken together, these findings indicate that ATE possesses a potential as a functional food with immunostimulatory activity.

Recently the importance of intellectual property has been increased. There has been various ways of research on analysis of companies, forecast of technology and so on through patents and many investments of money and time. Unlike traditional method of patent analysis such as company analysis, forecasting technologies, this research is to suggest the ways to forecast registration and rejection of patents which help minimize the efforts to register patents. To do so, information such as inventors, applicants, application date, and IPC codes were extracted to be used as input variables for analyzing Bayesian network. Especially, among various forms of Bayesian network, we used Tree Augmented NBN (TAN) to forecast registration and rejection of patent. This is because, TAN was assumed to have dependence between variables. As a result of this Bayesian network, it was shown that there are nearly more than 80% of accuracy to forecast registration and rejection of patents. Therefore, we expect the minimization of time and cost of registration by forecasting registration and rejection of R&D patent through this research.