Fig. 3: The upregulated SGLT1 supported the cell viability of the acquired TKI-resistant cells.
From: PKCδ-mediated SGLT1 upregulation confers the acquired resistance of NSCLC to EGFR TKIs
a The cell proliferation of H322/ER clones in response to erlotinib, phlorizin, or LX4211 was determined in WST-1 analysis. b The effects of phlorizin or LX4211 on cell viability of H322/ER clones under low glucose concentration were measured in WST-1 analysis. c, d The effects of SGLT1 shRNA on cell proliferation (c) and viability (d) of H322/ER clones under low glucose concentration were determined by cell counting and WST-1 analyses, respectively. e, f The effects of SGLT1 inhibitors (e) and shRNA (f) on caspase 3 or PARP cleavages or LC3β in H322/ER clones were analyzed by WB. g, h The effects of SGLT1 overexpression on the erlotinib-induced PARP and caspase 3 cleavages (g) and cell death (h) in H322 cells were examined in WB and WST-1 analyses, respectively. Data in (a)–(d), and (h) represent mean and sd from three independent experiments. *p < 0.05; **p < 0.01; ***p < 0.001 vs. control, Student’s t-test. Data in (e)–(g) are representative of three experiments.
