Fig. 1: Optogenetic probing of EML4-ALK+ cancer cells reveals suppression of RTK signaling.
From: Oncogenic EML4-ALK assemblies suppress growth factor perception and modulate drug tolerance
A EML4-ALK+ cancer cells treated with ALK inhibitors (ALKi) can persist through therapy and acquire stable drug resistance. B Immunofluorescence shows punctate expression of ALK in two EML4-ALK+ cancer cell lines. Scale = 10 µm. C Understanding functional interactions between EML4-ALK and transmembrane RTKs. D Functional profiling of RTK signaling in EML4-ALK+ cancer cells. E OptoFGFR allows blue-light-induced stimulation RTK/ERK signaling. F Single-cell immunofluorescence of ppERK levels in STE-1 cells stimulated with light (optoFGFR) in the presence (orange) or absence (gray) of ALK inhibitor crizotinib (ALKi, 1 µM). Significance assessed using one-sided KS test for difference of two distributions. G ppERK fold-change in response to 5 min of blue light stimulation over the range of the indicated stimulus intensities. Data points show the ratio of ppERK from stimulated and unstimulated cells. Each data point in (G) shows the mean of 3000–5000 cells. Error bars = 95% CI. See Supplementary Table 1 for biological and experimental replicate numbers for all experiments.
