Journal: Cancer cell

Article Title: Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS

doi: 10.1016/j.ccell.2018.08.009

Figure Lengend Snippet: (A) Percentage growth inhibition (x axis) of KL (red, A549 and H1944 cells), KLP (purple, HCC44, H23, H2122, and H2030 cells), and KP (blue, H2009, H441, and H358 cells) human NSCLC lines treated for 72 hr with 2.5 μM momelotinib or 10 nM trametinib plotted versus degree of baseline IL-6 secretion in conditioned medium (y axis). R2 values and p values for the correlation shown.

Article Snippet: Human: HCC44 , Broad Institute , N/A.

Techniques: Inhibition

Journal: Cancer cell

Article Title: Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS

doi: 10.1016/j.ccell.2018.08.009

Figure Lengend Snippet: (A) IB of the indicated proteins in A549, H1944, HCC44, H2009, H441, and H358 cells treated with or without 500 nM JQ1 for 24 hr. Red cell lines, KL; blue cell lines, KP.

Article Snippet: Human: HCC44 , Broad Institute , N/A.

Techniques:

Journal: Cancer cell

Article Title: Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS

doi: 10.1016/j.ccell.2018.08.009

Figure Lengend Snippet: (A) Crystal violet staining of A549, H1944, HCC44, H23, H2009, H1792, H441, and mouse embryonic fibroblast (MEF) cells In the presence of 2.5 μM MMB and 10 nM Tram each day and/or 500 nM JQ1 every other day (intermittent) for 12 days (See STAR Methods). Red cell lines, KL and KLP; blue cell lines, KP (upper). Quantification of extracted crystal violet in MMB + Tram + JQ1 treated cells was normalized to Tram + JQ1 treated cells (n = 3) (lower).

Article Snippet: Human: HCC44 , Broad Institute , N/A.

Techniques: Staining

Journal: Cancer cell

Article Title: Overcoming Resistance to Dual Innate Immune and MEK Inhibition Downstream of KRAS

doi: 10.1016/j.ccell.2018.08.009

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Human: HCC44 , Broad Institute , N/A.

Techniques: Control, Recombinant, Enzyme-linked Immunosorbent Assay, Cell Viability Assay, shRNA, Negative Control, Software, Binding Assay, Expressing

Journal: Pharmaceuticals

Article Title: New Genetic Bomb Trigger: Design, Synthesis, Molecular Dynamics Simulation, and Biological Evaluation of Novel BIBR1532-Related Analogs Targeting Telomerase against Non-Small Cell Lung Cancer

doi: 10.3390/ph15040481

Figure Lengend Snippet: Telomerase activity in cancer cells as a percent of control cells with target compounds 29a , 36b , and 39b .

Article Snippet: The human A549 (epithelial cell lung carcinoma, ATCC, Manassas, VA, USA), HCC44 (non-small cell lung adenocarcinoma, Leibniz Institute DSMZ-German Collection of the Microorganisms and the Cell Cultures, Braunschweig, Germany), and NCI-H23 (non-small cell lung adenocarcinoma, ATCC, Manassas, VA, USA) cell lines (compounds 29a , 36b , and 39b ) were diluted to 10 μM and incubated for 48 h before being tested using the TRAP method.

Techniques: Activity Assay, Control

Journal: medRxiv

Article Title: Potent clinical prognostic and systemic adjuvant therapeutic value of plasma fractalkine in PD-L1/PD-1 blockade immunotherapy for lung cancer

doi: 10.1101/2022.06.16.22276511

Figure Lengend Snippet: (a) The bar graphs show plasma concentrations of the selected proteins in responders (R, n=17, 26), progressors (PR, n=38, 59), hyperprogressors (HPR, n=3), patients with stable disease (SD, n=5, 11) and age-matched healthy donors (H, n=4, 6) before (baseline, B) and after the first cycle of immunotherapy (1C). Error bars are shown (standard deviations, SD), and relevant statistical comparisons by Mann-Whitney U tests are shown within the graphs. (b) Correlation between FKN plasma concentration and diversity index with Spearmańs test. (c) ROC analysis of FKN concentration as a predictor of objective responses. The calculated cut-off value for the statistics provided in the graph is shown. (d) Kaplan-Meier plot of PFS stratifying the patients according to the FKN cut-off value identified in the ROC curve (N=42). The associated P value is shown. (e) As in (d) but plotting OS. n= 46 (17 above the cut-off, 29 below). (f) Kaplan-Meier survival plot of lung adenocarcinoma (LUAD) patients. Patients were stratified according to FKN transcriptional expression level within tumor samples. Data were retrieved from the TCGA database and exported with TIMER2.0. Differences in survival were evaluated with the Log rank test, and associated P values are shown within the graph. n=515. HR=0.827; 95% confidence interval=0.784 to 0.945. (g) As in (f) but plotting squamous lung carcinoma (LUSC) patients n=501. HR=1.03; 95% confidence interval=0.885 to 1.095. (h) Real time cell growth (RTCA) of 3LL cell lines engineered to secrete the indicated cytokines. Relevant statistical comparisons of delta-cell indexes after 50 h of culture were carried out by ANOVA. (i) Bar graphs with cell growth rates for the indicated 3LL cell lines relative to the growth of unmodified 3LL cells. Error bars are shown (SD). Statistical comparisons by ANOVA and Tukeýs pairwise comparison tests are indicated. *, **, ***, indicate significant (p<0.05), very significant (p<0.01) and highly significant (p<0.001) differences; ns, non-significant differences.

Article Snippet: FKN concentration was quantified in a collection of 5 human lung adenocarcinoma cell lines (Calu6, H23, A549, HCC44, H358) and 5 human lung squamous carcinoma cell lines (H520, H1703, H226, H2170, SW900) from the American Type Culture Collection.

Techniques: Clinical Proteomics, MANN-WHITNEY, Concentration Assay, Expressing, Comparison

Journal: medRxiv

Article Title: Potent clinical prognostic and systemic adjuvant therapeutic value of plasma fractalkine in PD-L1/PD-1 blockade immunotherapy for lung cancer

doi: 10.1101/2022.06.16.22276511

Figure Lengend Snippet: (a) Evaluation of tumor infiltration with the indicated selected immune cell populations, and correlation analyses of FKN transcriptional expression and immune infiltrates from the TCGA database. Analyses were restricted to lung adenocarcinoma samples (n=515). Spearman correlation with different immune populations were identified by several algorithms (CIBERSORT, quanTIseq, xCell, TIDE) and an adjustment based on tumor purity was employed to minimize the potential interaction of low tumor cell quantities. Each dot represents a single tumor sample. Spearman’s rho value and p values are provided within the graphs. (b) Kaplan-Meier plot of OS according to FKN expression in a lung adenocarcinoma cohort registered in the TCGA database (n=240). Patients were stratified according to the median FKN expression value. Survival differences were tested by the Log rank test. Dotted lines represent 95% confidence intervals. (c) Correlation between tumor FKN and PD-L1 transcriptional expression by Spearmańs test. Relevant statistical results are presented within the graphs. (d) As in (c) but plotting PD-1 transcriptional expression levels.

Article Snippet: FKN concentration was quantified in a collection of 5 human lung adenocarcinoma cell lines (Calu6, H23, A549, HCC44, H358) and 5 human lung squamous carcinoma cell lines (H520, H1703, H226, H2170, SW900) from the American Type Culture Collection.

Techniques: Expressing

Journal: Bioengineered

Article Title: LncRNA SNHG12 in extracellular vesicles derived from carcinoma-associated fibroblasts promotes cisplatin resistance in non-small cell lung cancer cells

doi: 10.1080/21655979.2021.2018099

Figure Lengend Snippet: CAFs-EVs promoted DDP resistance in NSCLC cells. NSCLC cells were first co-cultured with CAFs-EVs or NFs-EVs, respectively, using the conditioned medium supplemented with GW4869 as the control, and then treated with different doses of DDP (0, 1, 2, 4, 6, 8, and 10 μg/mL). A: CCK-8 was used to test the NSCLC cell activity and the half inhibitory concentration (IC 50 ) of DDP; according to the results of the IC 50 values, A549 cells were treated with 6 μg/mL DDP, and HCC44 cells were treated with 5 μg/mL DDP; B: Colony formation assay was adopted to detect the proliferation of NSCLC cells; C: Flow cytometry was performed to examine the apoptotic level of NSCLC cells. The cell experiment was repeated 3 times independently, and data were expressed as mean ± standard deviation. Data in panels were analyzed using two-way ANOVA, followed by Tukey’s post-hoc test, * p < 0.05.

Article Snippet: NSCLC cell lines (A549 and HCC44) and human normal lung epithelial cell BEAS2B were procured from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Cell Culture, Control, CCK-8 Assay, Activity Assay, Concentration Assay, Colony Assay, Flow Cytometry, Standard Deviation

Journal: Bioengineered

Article Title: LncRNA SNHG12 in extracellular vesicles derived from carcinoma-associated fibroblasts promotes cisplatin resistance in non-small cell lung cancer cells

doi: 10.1080/21655979.2021.2018099

Figure Lengend Snippet: LncRNA SNHG12 was carried by CAFs-EVs into NSCLC cells. A: qRT-PCR was used to detect the expression of SNHG12 in human NSCLC cell lines (A549, HCC44) and human normal lung epithelial cell BEAS2B; B: qRT-PCR was performed to examine the expression of SNHG12 in CAFs-EVs or NFs-EVs and the expression of SNHG12 after the addition of GW4869 into CAFs or NFs; C: qRT-PCR was conducted to detect the expression of SNHG12 in NSCLC cells after CAFs-EVs treatment to A549 and HCC44; D: Rnase A or Rnase A in combination with Triton X-100 was conducted to treat CAFs-EVs, and qRT-PCR was used to detect the expression of SNHG12 in CAFs-EVs; E: CAFs transiently transfected with Cy3-SNHG12 were co-cultured with A549 or HCC44 44 cells for 48 h, and fluorescence microscope was used to verify the fluorescence signal in NSCLC cells. The cell experiment was repeated 3 times independently, and data were expressed as mean ± standard deviation. Data in panels A-B and D were analyzed using one-way ANOVA. Data in panel C were analyzed using two-way ANOVA, followed by Tukey’s post-hoc test, * p < 0.05.

Article Snippet: NSCLC cell lines (A549 and HCC44) and human normal lung epithelial cell BEAS2B were procured from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Quantitative RT-PCR, Expressing, Transfection, Cell Culture, Fluorescence, Microscopy, Standard Deviation

Journal: Bioengineered

Article Title: LncRNA SNHG12 in extracellular vesicles derived from carcinoma-associated fibroblasts promotes cisplatin resistance in non-small cell lung cancer cells

doi: 10.1080/21655979.2021.2018099

Figure Lengend Snippet: LncRNA SNHG12 carried by CAFs-EVs promoted the growth of NSCLC and DDP resistance in vivo . The nude mice were injected with A549 cell suspension to conduct a subcutaneous tumorigenesis experiment, then DDP (6 μg/mL, 4 mg/kg) and CAFs-NC-EVs or CAFs-oe-EVs overexpressing SNHG12 were intraperitoneally injected into nude mice. A: the volume of the tumor body within 15 d was measured; B: the weight of the tumor body on the 15th d was measured; C: IHC was performed to detect the positive rate of Ki67 in tumors; D: IHC was conducted to detect the positive rate of HuR in tumors; E-F: qRT-PCR was used to detect the levels of SNHG12 and XIAP in vivo . N = 6; the cell experiment was repeated 3 times independently, and data were expressed as mean ± standard deviation. Data in panel A was analyzed using two-way ANOVA and data in panels B-F were analyzed using one-way ANOVA, followed by Tukey’s post-hoc test, * p < 0.05.

Article Snippet: NSCLC cell lines (A549 and HCC44) and human normal lung epithelial cell BEAS2B were procured from American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: In Vivo, Injection, Suspension, Quantitative RT-PCR, Standard Deviation