Mercury bioaccumulation and assimilation in marine plankton in meltwater influenced fjords and shelf waters along the east coast of Greenland.

The rapid melting of the Arctic cryosphere due to climate change will result in significant freshwater input into Arctic marine ecosystems. This might also cause the release of legacy mercury (Hg) stored in the cryosphere, increasing Hg concentration and its subsequent effects on the marine biota. However, there is scarce knowledge on the concentration of Hg in the lower trophic level organisms at the base of the Arctic pelagic food web.

Loss of the predicted cell adhesion molecule MPZL3 promotes EMT and chemoresistance in ovarian cancer.

Myelin protein zero-like 3 (MPZL3) is an Immunoglobulin-containing transmembrane protein with predicted cell adhesion molecule function. Loss of 11q23, where the gene resides, is frequently observed in cancer, and copy number alterations are frequently detected in tumor specimens. Yet the role and consequences of altered MPZL3 expression have not been explored in tumor development and progression.

Stress response regulation of mRNA translation: Implications for antioxidant enzyme expression in cancer.

From tumorigenesis to advanced metastatic stages, tumor cells encounter stress, ranging from limited nutrient and oxygen supply within the tumor microenvironment to extrinsic and intrinsic oxidative stress. Thus, tumor cells seize regulatory pathways to rapidly adapt to distinct physiologic conditions to promote cellular survival, including manipulation of mRNA translation. While it is now well established that metastatic tumor cells must up-regulate their antioxidant capacity to effectively spread and that regulation of antioxidant enzymes is imperative to disease progression, relatively few studies have assessed how translation and the hijacking of RNA systems contribute to antioxidant responses of tumors.

Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.

Quiescence is a reversible cell cycle exit traditionally thought to be associated with a metabolically inactive state. Recent work in muscle cells indicates that metabolic reprogramming is associated with quiescence. Whether metabolic changes occur in cancer to drive quiescence is unclear.