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. 2022 Apr 29;14(9):2222. doi: 10.3390/cancers14092222

Figure 1.

Figure 1

LPIN1 depletion increases gefitinib sensitivity by enhancing apoptosis in TKI-resistant NSCLC cells. (A) H1650 cells stably transduced with a lentiviral vector carrying shLPIN1 (H1650/shLPIN1) or shControl (H1650/pLKO) were treated with gefitinib or DMSO for 120 h. The gefitinib sensitivity of each cell line was determined using varying gefitinib concentrations. (B) H1650 cells were transfected with siRNAs for LPIN1 and then treated with gefitinib or DMSO for 120 h. The gefitinib sensitivity of each cell line was determined using varying gefitinib concentrations. (C) H1650 cells were infected with shLPIN1- or pLKO-harboring lentivirus and treated with gefitinib (10 μM) or DMSO for 10 days. Cell growth was measured by a colony formation assay after 0.5% crystal violet staining. (D) H1650 and HCC827 cells were infected with shLPIN1- or pLKO-harboring lentivirus and treated with gefitinib (10 μM in H1650 or 1 nM in HCC827 cells) or DMSO for 14 days. Cell growth was measured by an anchorage-independent growth assay in soft agar. (E) H1650 cells were transfected with siRNAs for LPIN1; treated with gefitinib (5 μM) or DMSO for 72 h; harvested; stained with Annexin-V, Alexa Fluor® 647 conjugate, and PI; and analyzed via flow cytometry. Etoposide (100 μM) was used as the positive control for inducing apoptosis. (F) Levels of proteins including cleaved PARP and caspase-3 were analyzed via western blotting. β-Actin was used as a loading control. Values are the means ± SD of three independent experiments. Statistical significance was determined by Student’s t-test (*, p < 0.05 and NS, not significant).