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usage. To start with, high-grade brain tumors are characterized by low activity of adenylyl cyclase and/or depletion of cytoplasmic cAMP. Concomitantly, glioma and astrocytoma cell lines like A-172 and 1321N1 are highly susceptible to increased production of cAMP, which can be achieved by treatment with cAMP analogues, adenylyl cyclase activators or phosphodiesterase inhibitors (Chen et al. 1998; Toll et al. 2011). It is not surprising that agonists of β-AR can mimic the antiproliferative effects of the above-mentioned compounds, as canonical β-AR signaling pathway involves the Gs-dependent activation of adenylyl cyclase and subsequent accumulation of cAMP (Toll et al. 2011). In our study carried out in 1321N1 cells, the level of cAMP induced by the β2-AR agonists like fenoterol and isoproterenol positively correlated with decreased mitogenesis (Fig. 1). Similarly, decreased cell growth was observed in response to β-AR agonists in nontumor breast MCF-10A cells (Bruzzone et al. 2014) and in breast cancer cell line MDA-MB-231 (Carie and Sebti 2007). In significance, Gargiulo et al. demonstrated that β2-AR knock-down led to increase of cell proliferation and migration of MCF-7 breast cancer cell line, indicating that β2-AR exerts an inhibitory tone towards cell growth and motility at basal conditions (Gargiulo et al. 2014). When the same cell line was engineered to overexpress β2-AR, significant drop in cell growth and migration was observed (Gargiulo et al. 2014). In line with this work, our unpublished data on rat C6 glioma cells indicate that siRNA-mediated depletion of β2-AR leads to significant increase in phosphoactive forms of AKT and ERK1/2. Taken together, expression level of the β2-AR receptor is an important factor shaping the proliferative capacity of cancer cells, and should be taken into account when studying the cellular responses to β2-AR ligands. To Editor,