Accumulating evidence has revealed that thePI3K/AKT/PTENpathway acts as a pivotal determinant of cell fate regarding senescence and apoptosis, which is mediated by intracellular reactive oxygen species (ROS) generation. NADPH oxidase (NOX) family of enzymes generates the ROS. The regulation of NOX enzymes is complex, with many members of this family exhibiting complexity in terms of subunit composition, cellular location, and tissue-specific expression. Cells are continuously exposed to the ROS, which represent mutagens and are thought to be a major contributor to several diseases including cancer and aging process. Therefore, cellular ROS sensing and metabolism are firmly regulated by a variety of proteins involved in the redox mechanism. In this review, the roles of oxidative stress in PI3K/AKT/PTEN signaling are summarized with a focus on the links between the pathways and NOX protein in several diseases including cancer and aging.
In various terrestrial and aquatic ecosystems, predators affect resources indirectly via intermediate prey. Such indirect interactions involve reducing the density of the prey (density-mediated indirect interactions, DMIIs) or changing the behavioral, morphological, or life history traits of the prey (trait-mediated indirect interactions, TMIIs). Although the importance of TMIIs has been highlighted recently, the strengths of both DMIIs and TMIIs under natural conditions have rarely been evaluated, especially in the context of resource community structure. We studied a three-level marine food chain involving the carnivorous snail Thais clavigera, its limpet prey Siphonaria sirius, and the limpet's food sources, the algae Lithoderma sp. and Ulva sp. We measured the strengths of DMIIs and TMIIs and observed how the algal community changes under the pressure of natural predation by T. clavigera on S. sirius. Neither DMIIs nor TMIIs affected the total algal cover or chlorophyll content per unit area. However, both types of indirect interactions caused similar changes in algal composition by increasing the cover of Ulva and decreasing the cover of Lithoderma. This change in the algal community was caused by a reduction in the limpet's preferential consumption of the competitively dominant Ulva over Lithoderma. These results suggest that both DMIIs and TMIIs have similar effects on the changes in resource community structure under natural conditions.
Most of the Parkinson disease (PD) linked genes are also associated with cancers. In particular, phosphatase and tensin homologue-induced kinase 1 (PINK1) and Parkin, both of which are involved in recessively inherited familial forms of PD linked to mitochondrial dysfunction, appear to be abnormally expressed in cancers. Functional studies have revealed that PINK1 recruits Parkin to mitochondria to initiate mitophagy, an important autophagic quality control mechanism that rids the cell of damaged mitochondria. Although PD and cancer are obviously disparate human disorders, there is an evidence for low cancer rates in patients with PD. The relationship between cancer rates and PD might be related to the involvement of common pathways in both diseases. This paper provides a concise overview on the cellular functions of the PINK1 and Parkin.
Multiple enzymes participate in the phosphorylation of a group of phosphoinositide lipids. Because of their important role in signal transduction, the dysregulated metabolism of phosphoinositides represents a key step in many disease settings. Loss of their function has been demonstrated to occur as an early event a wide variety of carcinogenesis and has therefore been suggested as a biomarker for the premalignant disease. In addition, genetic alterations at multiple nodes in the pathway have been implicated in several other diseases. Accordingly, given this pervasive involvement in many diseases, the development of molecules that modulates this pathway has been initiated in studies. They have been the focus of extensive research and drug discovery activities. A better understanding of the molecular connections could uncover new targets for drug development.
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