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. Author manuscript; available in PMC: 2016 Nov 17.
Published in final edited form as: Adv Lung Cancer (Irvine). 2016 Jan 28;4(3):37–51. doi: 10.4236/alc.2015.43006

Figure 3.

Figure 3

(a) Bulk tumor cells and tumor stem cells were isolated from a patient with lung cancer and analyzed by western blot for PGRMC1 (upper panel) and GAPDH (lower panel, loading control). PGRMC1 was abundant in both the bulk tumor cells and the stem cells; (b) Cancer-derived stem cells were treated with various ligands and assayed for viability. Neither the EGFR inhibitor erlotinib nor the ERK inhibitor PD98059 were active against the cells, while the PGRMC1 ligand AG-205 inhibited viability of the cells; (c) Bright field imaging of cancer-derived stem cells treated with AG-205 revealed cell rounding in the majority of the cells. d Western blot analysis of stem cells treated with vehicle (lane 1) or AG-205 (lane 2) revealed increased levels of the autophagy initiating protein LC3B-II (top panel, lower band), while the levels of the autophagy substrate p62 were unchanged (second panel). PGRMC1 levels increased following treatment (third panel), and GAPDH served as a loading control.