Journal: Cancer Research

Article Title: Epithelial to Mesenchymal Transition Is a Determinant of Sensitivity of Non–Small-Cell Lung Carcinoma Cell Lines and Xenografts to Epidermal Growth Factor Receptor Inhibition

doi: 10.1158/0008-5472.can-05-1058

Figure Lengend Snippet: Figure 3. A, NSCLC lines were grown as s.c. xenografts in nu/nu mice and dosed for 14 days with erlotinib (100 mg/kg qd) or vehicle control. Statistical evaluation of percent tumor growth inhibition by repeated measures ANOVA was done. H292, H358, and H441 were found to be sensitive to EGFR inhibition in vivo. No correlation between tumor growth rate and sensitivity to EGFR inhibition was observed. Solid bars, erlotinib dosing period. B, tumor cell lysates were evaluated for the expression of epithelial and mesenchymal proteins. Tumors were grown to a volume of f300 mm3, excised, and flash frozen in liquid nitrogen. Tumor tissues were pulverized while frozen, subjected to detergent lysis and SDS-PAGE as described, and immunoblots probed with antibodies to E-cadherin, h-catenin, Brk, fibronectin, and vimentin. Similar with in vitro results, E-cadherin expression was restricted to erlotinib-sensitive lines and vimentin to insensitive lines. Antibody to GAPDH was used as a loading control.

Article Snippet: The human NSCLC lines (H292, H358, H322, H441, A549, Calu6, H460, H1703, SW1573, Calu3, Colo699, H2122, A427, H1437, H1299, Hop92, and H23) were cultured in the appropriate American Type Culture Collection recommended supplemented media.

Techniques: Control, Inhibition, In Vivo, Expressing, Lysis, SDS Page, Western Blot, In Vitro

Journal: Oncogene

Article Title: Identification of putative oncogenes in lung adenocarcinoma by a comprehensive functional genomic approach.

doi: 10.1038/sj.onc.1209289

Figure Lengend Snippet: Figure 2 EEF1A2 amplification is associated with high EEF1A2 protein expression in lung adenocarcinomas. (a) Cells from a lung adenocarcinoma sample in which EEF1A2 is amplified show more green signals (EEF1A2) than red signals (chromosome 20 centromeric probe) (original magnification, 400). (b) Immunohistochemical staining of cells from the same tissue sample as in panel a shows strong EEF1A2 staining in the cytoplasm. (c) A lung adenocarcinoma sample with two copies of EEF1A2 and chromosome 20 centromeric probe, indicating no EEF1A2 amplification (original magnification, 400). (d) Immunohistochemical staining of cells from the same tissue sample as in panel c shows negative staining for EEF1A2.

Article Snippet: Six human lung adenocarcinoma cell lines (H23, H229, H1792, SK-LU-1, H522, and H1563) were obtained from the American Type Culture Collection (Manassas, VA, USA).

Techniques: Expressing, Immunohistochemical staining, Staining, Negative Staining

Journal: Cell metabolism

Article Title: Oncogene amplification in growth factor signaling pathways renders cancers dependent on membrane lipid remodeling

doi: 10.1016/j.cmet.2019.06.014

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Human: H23 , ATCC , CRL-5800.

Techniques: Recombinant, Membrane, Transfection, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Negative Control, Empire Assay, Plasmid Preparation, shRNA, Control, Sequencing, Software

Journal: Journal of Oncology

Article Title: Enhancing the Therapeutic Efficacy of KRAS G12C Inhibitors in Lung Adenocarcinoma Cell Models by Cotargeting the MAPK Pathway or HSP90

doi: 10.1155/2021/2721466

Figure Lengend Snippet: FGFR1 is involved in resistance to KRAS G12C inhibitors in NSCLC cells. (a) CCK-8 assay showing the dose viability responses of NSCLC cell lines treated with ARS-1620 ( ∗ p < 0.05; ∗∗ p < 0.01). (b) Real-time PCR analysis of the FGFR1 levels in H358, H23, and Calu-1 cells. (c) Western blot analysis of FGFR1 and p-FGFR1 in H358, H23, and Calu-1 cells, with β -actin serving as a loading control. ((d)-(f)) CCK-8 assays of H358, H23, and Calu-1 cells treated with ARS-1620, AZD4547, or both. (g) Viability of control H358 cells (H358-CON) and H358 cells overexpressing FGFR1 (H358-FGFR1 OE ) as determined by the CCK-8 assay. (h) CCK-8 assays of H358-FGFR1 OE cells treated with ARS-1620, AZD4547, or both. (i) Western blot analysis of S6, p-S6, ERK, and p-ERK in H358, H23, Calu-1, and H358-FGFR1 OE cells treated with ARS-1620, AZD4547, or both, with catenin or β -actin serving as a loading control. All data in the bar graphs of figures are the mean ± SD ( n ≥ 3). ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: H358, Calu-1, and H23 cells were obtained from ATCC (Manassas, VA, USA).

Techniques: CCK-8 Assay, Real-time Polymerase Chain Reaction, Western Blot, Control

Journal: Journal of Oncology

Article Title: Enhancing the Therapeutic Efficacy of KRAS G12C Inhibitors in Lung Adenocarcinoma Cell Models by Cotargeting the MAPK Pathway or HSP90

doi: 10.1155/2021/2721466

Figure Lengend Snippet: Cotargeting the MAPK pathway and HSP90 enhances the anticancer activity of KRAS G12C inhibitors. (a) CCK-8 viability assay of H358 cells treated with the indicated drug combinations at low or high concentrations. (b) Crystal blue staining of H358 cells treated with ARS-1620 or ARS-1620 in combination with PD0325901 at low or high concentrations. (c) Volumes of H358 xenograft tumors ( n = 5 for each group) treated with vehicle, AMG 510, AMG 510 + trametinib, or AMG 510 + trametinib + AZD4547. (d) Viability assay of H358_P and H358_R cells treated with ARS-1620 and GDC-094. (e) Viability assay of H358_R cells treated with ARS-1620, STA-9090, or both. (f) Viability analysis of STA-9090 as a single agent in a panel of lung cancer cells and A375 melanoma cells. (g) Volumes of H358 xenograft tumors treated with vehicle, AMG 510, STA-9090, or the two agents in combination ( n ≥ 5). (h) Viability assay of H358 and H358_R cells treated with AMG 510, STA-9090, or both for 72 h. ((i)-(j)) Viability assay of H23 and Calu-1 cells treated with AMG 510, STA-9090, or both for 48 or 72 h. (k) Western blot analysis of AKT, p-AKT, S6, p-S6, ERK, and p-ERK in H358, H23, Calu-1, and H358_R cells treated with AMG 510, STA-9090, or both for 24 h with catenin serving as a loading control.

Article Snippet: H358, Calu-1, and H23 cells were obtained from ATCC (Manassas, VA, USA).

Techniques: Activity Assay, CCK-8 Assay, Viability Assay, Staining, Western Blot, Control