Functional synergism of pyoverdine and the S-type pyocins of Pseudomonas aeruginosa / 生物工程学报

Pyocin S2 and S4 in Pseudomonas aeruginosa use the same uptake channels as the pyoverdine does in bacteria, indicating a possible connection between them. In this study, we characterized the single bacterial gene expression distribution of three S-type pyocins (Pys2, PA3866, and PyoS5) and examined the impact of pyocin S2 on bacterial uptake of pyoverdine. The findings demonstrated that the expression of the S-type pyocin genes was highly differentiated in bacterial population under DNAdamage stress. Moreover, exogenous addition of pyocin S2 reduces the bacterial uptake of pyoverdine so that the presence of pyocin S2 prevents the uptake of environmental pyoverdine by non-pyoverdine synthesizing 'cheaters', thereby reducing their resistance to oxidative stress. Furthermore, we discovered that overexpression of the SOS response regulator PrtN in bacteria significantly decreased the expression of genes involved in the synthesis of pyoverdine, significantly decreasing the overall synthesis and exocytosis of pyoverdine. These findings imply a connection between the function of the iron absorption system and the SOS stress response mechanism in bacteria.

ROS-mediated mechanisms：an anticancer strategy / 中国生化药物杂志

Under the influence of oncogenic signals and abnormal metabolism, the redox status of cancer cells often differs from that of the normal cells, manifesting as elevated generation of reactive oxygen species( ROS) and oxidative stress.Many signaling pathways involved in tumorigenesis can directly or indirectly regulate ROS metabolism.Currently, the biological significance of increased ROS in cancer cells is still somewhat controversial.ROS on the one hand can promote cancer development and drug resistance, and on the other hand can also cause cell injury and even cell death.To maintain cell viability and proliferation, cancer cells usually up-regulate their antioxidant capacity in adaptation to the intrinsic oxidative stress.Such adaptive mechanisms to oxidative stress are highly important in both cancer development and also play a major role in cancer cell response to therapy.Compelling evidences from recent studies have suggested that targeting the redox regulation mechanisms through proper intervention strategies may have significant therapeutic implications in cancer treatment.This article will focus on alterations of redox status in cancer cells, their adaptation to oxidative stress, and the underlying mechanisms.Potential therapeutic strategies based on such biochemical characteristics of cancer cells will also be discussed.