Figure 2.

Pancreatic cancer cell derived membranes stimulate ERK1/2 phosphorylation in MCs by a CD73-dependent mechanism. LAD2 cells (1 × 10⁶ cells/mL) were incubated for 30 min in the absence or presence of APCP (5 μM). Cells were then left untreated or treated for 1 min with membranes derived from Mia PaCa-2 pancreatic cancer cells (50 μg/mL), as indicated. Cell lysates were resolved by SDS-PAGE and immunoblotted with anti phospho-ERK1/2 antibodies, followed by reprobing with anti-total-ERK2 as indicated. A representative blot is shown. The intensities of the bands corresponding to phospho-ERK1/2 and total-ERK2 were quantified by densitometry using Image-J software and the relative pixel densities (phosphorylated/total) were calculated. Data are presented as mean ± SEM of three independent experiments. ** p = 2.0 × 10⁻⁷. “Reprinted from Cancer Letters, 397, Yaara Gorzalczany, Eyal Akiva, Ofir Klein, Ofer Merimsky and Ronit Sagi-Eisenberg, Mast cells are directly activated by contact with cancer cells by a mechanism involving the autocrine formation of adenosine and autocrine/paracrine signaling of the adenosine A3 receptor. 23-32, Copyright © 2017 with permission from Elsevier.”