Metatranscriptomic insights into the microbial electrosynthesis of acetate by Fe2+/Ni2+ addition.

As important components of enzymes and coenzymes involved in energy transfer and Wood-Ljungdahl (WL) pathways, Fe2+ and Ni2+ supplementation may promote the acetate synthesis through CO2 reduction by the microbial electrosynthesis (MES). However, the effect of Fe2+ and Ni2+ addition on acetate production in MES and corresponding microbial mechanisms have not been fully studied. Therefore, this study investigated the effect of Fe2+ and Ni2+ addition on acetate production in MES, and explored the underlying microbial mechanism from the metatranscriptomic perspective. Both Fe2+ and Ni2+ addition enhanced acetate production of the MES, which was 76.9% and 110.9% higher than that of control, respectively. Little effect on phylum level and small changes in genus-level microbial composition was caused by Fe2+ and Ni2+ addition. Gene expression of 'Energy metabolism', especially in 'Carbon fixation pathways in prokaryotes' was up-regulated by Fe2+ and Ni2+ addition. Hydrogenase was found as an important energy transfer mediator for CO2 reduction and acetate synthesis. Fe2+ addition and Ni2+ addition respectively enhanced the expression of methyl branch and carboxyl branch of the WL pathway, and thus promoted acetate production. The study provided a metatranscriptomic insight into the effect of Fe2+ and Ni2+ on acetate production by CO2 reduction in MES.

The hypoxia-related signaling pathways of vasculogenic mimicry in tumor treatment.

Tumors require a blood supply for survival, growth, and metastasis. It is widely accepted that the development of the tumor microcirculation compartment need the production of new blood vessels (angiogenesis). Vasculogenic mimicry (VM) is an alternative type of blood supplement independent of endothelial vessels which refers to the formation of tumor cell-lined vessels and is associated with tumor invasion, metastasis and poor cancer patient prognosis. Although a variety of proteins and microenvironmental factors are known to contribute to VM, the mechanisms underlying its formation remain unclear. The induction of VM seems to be related to hypoxia, which may promote the plastic, transendothelial phenotype of tumor cells capable of VM. Here, with regard to the above aspects, we review the advanced research on VM including molecular mechanisms and its clinical significance; and explore the development of VM-related strategies which are being utilized for anticancer treatment.