No abstract

Several questions about the role of the oxygen sensor prolyl-hydroxylase 2 (PHD2) in cancer have not been addressed. First, the role of PHD2 in metastasis has not been studied in a spontaneous tumor model. Here, we show that global PHD2 haplodeficiency reduced metastasis without affecting tumor growth. Second, it is unknown whether PHD2 regulates cancer by affecting cancer-associated fibroblasts (CAFs). We show that PHD2 haplodeficiency reduced metastasis via two mechanisms: (1) by decreasing CAF activation, matrix production, and contraction by CAFs, an effect that surprisingly relied on PHD2 deletion in cancer cells, but not in CAFs; and (2) by improving tumor vessel normalization. Third, the effect of concomitant PHD2 inhibition in malignant and stromal cells (mimicking PHD2 inhibitor treatment) is unknown. We show that global PHD2 haplodeficiency, induced not only before but also after tumor onset, impaired metastasis. These findings warrant investigation of PHD2's therapeutic potential.

Plasma-enhanced (PE)CVD is used to create, in a single step, a superhydrophobic (SH) (water contact angle over 1508) layer starting from hexamethyldisiloxane (HMDSO) vapor (i.e., without fluorine) in a low-frequency, capacitively coupled plasma reactor under low pressure. Several SH microstructures are obtained, depending on experimental parameters (gas pressures, substrate rotation, pulsed glow discharge, plasma duration) deposited on various substrate types. The presented technique can produce thin SH transparent films (below 1 mm) or thicker ones (above 10 mm) to modify the surface of a macroporous hydrophilic membrane in order to render it SH with a water transmembrane pressure close to 2 bar.