13 research outputs found

    Additional file 1: of RNA-Seq profiling of circular RNAs in human laryngeal squamous cell carcinomas

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    Table S1. Demographic characteristics of patients with LSCC involved in this study. Table S2. Individual circRNAs detected in the study (please see the attached excel spreadsheet). Table S3. LSCC specific circRNAs detected in the study (please see the attached excel spreadsheet). Figure S1. The representative images of H&E-stained normal laryngeal mucosal and LSCC specimens. Pictures included well differentiated (upper), moderately differentiated LSCC (middle), and normal tissues (lower). From left to right, image magnifications of 40×, 100×, 200×, and 400 × were displayed (scale bar = 100 μm). Figure S2. Gene Ontology annotation analysis for 20 circRNA interacted miRNA and their target gene related significant enriched biological process, cellular components and molecular function. Figure S3. KEGG analysis showing the map of pathway in LSCC using the dysregulated circRNA-miRNA-target genes. (ZIP 8463 kb

    Oxygen consumption rates differentially altered upon drug perturbation in sensitive compared to insensitive cells.

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    <p>(A) NCI-H358 epithelial and mesenchymal lines or (B) NCI-H1703 (BPTES sensitive) and NCI-H1563 (BPTES insensitive) cells were treated with DMSO or 8 µM BPTES and oxygen consumption rate (OCR) was monitored over a 20 hr treatment. Data normalized to OCR at time zero (100%) and presented as mean values +/−SEM. <i>P</i> = 0.024 comparing changes in oxygen consumption with BPTES in the epithelial vs mesenchymal line; <i>P</i> = 0.00017 comparing NCI-H1703 and NCI-H1563 cells. (C) OCR following treatment with the indicated drugs to perturb mitochondrial respiration. Data normalized to OCR measurement prior to oligomycin treatment. (D) Addition of pyruvate to media restores the impaired FCCP response in the mesenchymal line. Average values +/−SEM indicated. Results representative of 2–3 independent experiments.</p

    Cell line panel screen and validation of BPTES as an on-target tool compound.

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    <p>(A) Sensitivity of a panel of NSCLC lines to inhibition of growth by 10 µM BPTES in a 72 hr proliferation assay. Growth rates (mu) plotted relative to DMSO control for each cell line (mu/max). (B,C) A427 parent cells or cells stably expressing an empty vector control (Con), wild-type GAC (GAC), or a BPTES-resistant GAC enzyme (GAC-BR) were treated with the indicated concentrations of BPTES (A) or the inactive BPTES analogue, AGX-4769 (C), in a 72 hr proliferation assay. Results are representative of three independent experiments with mean and standard deviation indicated. (D,E) Measurement of isotopomer labeled <sup>13</sup>C(5)-Glu (D) or <sup>13</sup>C(4)-Asp (E) from cells treated for 4 hr with BPTES or with inactive analogue AGX-4769. Results are the mean of three replicates with the standard deviation indicated. Calculated p-values from student t-test, <sup>*</sup>(3×10<sup>−8</sup>), <sup>**</sup>(10<sup>−9</sup>), <sup>#</sup>(10<sup>−7</sup>), <sup>##</sup>(2×10<sup>−6</sup>).</p
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