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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: Nrf2 activation drive macrophages polarization and cancer cell epithelial-mesenchymal transition during interaction

Fig. 4

Lactate elevated intracellular ROS of macrophages to induce M2 TEM formation through Nrf2. a macrophages were incubated with 2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA) for 30 mins, then stimulated with FBS-free medium (Neg Ctrl), the normal cancer cell CM (Ctrl), oxalic acid pre-treated cancer cell CM (OA), or exogenous lactate supplement contained oxalic acid pre-treated cancer cell CM (OA + LA) for another 6 h, the fluorescent intensity of 2′,7′-dichlorofluorescein (DCF) were detected (n = 4). b macrophages were incubated with 2′,7′-dichlorodihydrofluorescein diacetate (H2DCFDA) for 30 mins, then stimulated with normal cancer cell CM with (NAC) or without NAC (Ctrl). The fluorescent intensity of 2′,7′-dichlorofluorescein (DCF) was detected (n = 4). c the nuclear Nrf2 of macrophages after stimulation by cancer cell CM with or without NAC was measured by western blot. d M1/2 macrophages markers expression of TEM induced by cancer cell CM or cancer cell CM and NAC (n = 4). e 24-h secretion of IL-1, IL-6 and VEGF of macrophages stimulated by cancer cell CM with or without NAC (n = 3). Graphs show the data as mean ± SD. *, P < 0.05, compared between two groups or with ctrl. N.S., no significant between two groups

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