Estrogens desensitize MCF-7 breast cancer cells to apelin-induced autophagy and enhanced growth under estrogen starvation: a possible implication in endocrine resistance.

Apelin-13 is an adipokine known for its growth-inducing effects on human breast cancer cells in an estrogen-containing environment. However, the response of these cells to apelin-13 in the absence of estrogen and its association with the expression of the apelin receptor (APLNR) has not yet been investigated. In the present study, we show that the breast cancer cell line MCF-7 expresses the APLNR as shown by immunofluorescence and flow cytometry, under conditions of ER starvation and that culture of these cells in the presence of apelin-13 results in an increased growth rate and a diminished autophagy flux.

A class IA PI3K controls inflammatory cytokine production in human neutrophils.

Neutrophils are generally the first leukocytes to arrive at sites of inflammation or injury, where they release a variety of inflammatory mediators, which contribute to shaping the ensuing immune response. Here, we show that in neutrophils exposed to physiological stimuli (i.e.