scholarly journals Increased EGFR Phosphorylation Correlates with Higher Programmed Death Ligand-1 Expression: Analysis of TKI-Resistant Lung Cancer Cell Lines

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Kenichi Suda ◽  
Leslie Rozeboom ◽  
Koh Furugaki ◽  
Hui Yu ◽  
Mary Ann C. Melnick ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell ◽  
Programmed Death Ligand 1 ◽  
Programmed Death ◽  
L1 Protein

Despite the recent development of immunotherapies that target programmed death-1 (PD-1) or programmed death ligand-1 (PD-L1) in non-small cell lung cancer (NSCLC) treatment, these therapies are less effective in NSCLC patients with epidermal growth factor receptor (EGFR) mutations. However, the molecular mechanisms underlying this lower efficacy of immunotherapies in EGFR mutant lung cancers are still unclear. In this study, we analyzed PD-L1 protein expression in lung cancer cell lines with EGFR mutations prior to and after acquisition of resistance to EGFR tyrosine kinase inhibitors (TKIs). We found that parental lung cancer cell lines harboring EGFR mutations showed negative (PC9 and H3255 cells) and positive (HCC827 cells) staining for PD-L1 by immunohistochemistry. Comparing PD-L1 expression between EGFR-TKI resistant cell lines and their parental cells, we found that increased phosphorylation of EGFR was related to increased expression of PD-L1. Increased phosphorylation of EGFR was accompanied by the T790M secondary mutation. Acquired resistance cells with MET amplification or EGFR loss both showed decreased phosphorylation of EGFR and decreased PD-L1 expression. Our results indicate that lung cancer cell lines with EGFR mutations (parental cells) do not harbor high PD-L1 protein expression. In addition, EGFR phosphorylation affects PD-L1 expression after acquisition of resistance to EGFR-TKIs.

scholarly journals Differentiating responses of lung cancer cell lines to Doxorubicin exposure:in vitroRaman micro spectroscopy, oxidative stress and bcl-2 protein expression

2016 ◽  
Vol 10 (1) ◽  
pp. 151-165 ◽  
Author(s):  
Zeineb Farhane ◽  
Franck Bonnier ◽  
Marcus Alexander Maher ◽  
Jane Bryant ◽  
Alan Casey ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Protein Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell

Evaluation of CD73 in lung cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14525-e14525
Author(s):  
Hui Yu ◽  
Maya Amar ◽  
Christopher J Rivard ◽  
Kim Ellison ◽  
Leslie Rozeboom ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Cancer Patients ◽  
Cell Lines ◽  
Cancer Cell ◽  
Genomic Data ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell ◽  
Lung Cancer Patients ◽  
Cd73 Expression

e14525 Background: Immunotherapy has shown promising results in multiple forms of cancer including lung cancer patients. Treatment targeting alternative immune checkpoints may demonstrate value for specific cancers or in combination therapy with other immunotherapies or chemotherapeutic agents. While adenosine has physiological importance in preventing excess inflammatory reactions and inhibiting autoimmunity, it is generated through an enzymatic cascade in the tumor microenvironment whereby AMP is ultimately dephosphorylated to adenosine by CD73 on tumor cells. Previous studies have shown that increased tumor CD73 expression correlated with increased metastasis, worse prognosis and chemotherapy resistance. Methods: Genomic data from the CCLE and TCGA database were evaluated for CD73 expression in lung cancer. The specificity of an anti-CD73 antibody (Cell Signaling) was confirmed by Western blotting in lung cancer cell lines. Immunohistochemistry (IHC) was performed for FFPE lung cancer cell lines and a NSCLC patient cohort. CD73 expression data was correlated with patient demographic data including outcomes. Results: CD73 mRNA was expressed in lung cancer cell lines (70/126, 55.6%) and did not correlate with other immune checkpoint ligands including PD-L1, GAL-9, and B7H4 in NSCLC. Review of the TCGA database identified CD73 expression is highest in thyroid carcinoma and significant in lung cancer. The prevalence of CD73 protein expression by IHC in NSCLC cell lines was 84.8% (39/46) and 15.4% (6/39) in SCLC cell lines. We also evaluated CD73 protein expression in a NSCLC cohort with a prevalence of 32.1% (36/112), with no significant correlation to patient clinical characteristics or outcomes. Conclusions: We evaluated the expression of the immune checkpoint, CD73, in lung cancer cell lines and tissues. Both genomic data and protein expression by IHC demonstrated CD73 was significantly expressed. However, there was no correlation with other immune biomarkers or patient demographics or outcomes. CD73 is a new target for immunotherapy and current clinical studies with CD73 inhibitors may prove beneficial to lung cancer patients.

scholarly journals The Clinical Influence of Autophagy-Associated Proteins on Human Lung Cancer

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Yuan Chen ◽  
Kai Leonie Schnitzler ◽  
Yunxia Ma ◽  
Miljana Nenkov ◽  
Bernhard Theis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Methylation ◽  
Protein Expression ◽  
Cell Lines ◽  
Cancer Cell ◽  
Lung Tumor ◽  
Cancer Cell Lines ◽  
Beclin 1 ◽  
Lung Cancer Cell ◽  
Associated Proteins

Exploitation of autophagy might potentially improve therapeutic strategy. Here, we analyzed the protein expression of autophagy-associated genes including LC3A, LC3B, Beclin-1, p62, and Atg5 in 88–131 primary lung tumors by immunohistochemistry (IHC) on tissue-microarrays (TMAs). Additionally, the DNA methylation pattern of LC3A was investigated by bisulfite sequencing (BS) and methylation-specific-PCR (MSP). It turned out that the higher expression of LC3A protein was associated with adenocarcinoma compared to squamous cell carcinoma of lung (p=0.008), positive staining of LC3B was significantly related to tumor grade (p=0.006), and the protein expression of Beclin-1 was significantly correlated to pN stage (p=0.041). The expression of p62 and Atg5 was however not significantly associated with any clinicopathological parameters. Downregulation of LC3A was related to DNA methylation in lung cancer cell lines, while in primary lung tumor samples, protein expression of LC3A was not significantly correlated with DNA methylation, and the methylation status of LC3A was not related to clinicopathological features. Taken together, our results suggest that autophagy-associated proteins such as LC3A, LC3B, and Beclin-1 might be potential biomarkers for subclassification, differentiation, and local metastasis in primary lung tumor, and epigenetic mechanism is partially responsible for gene silencing of LC3A in lung cancer cell lines.

scholarly journals Diclofenac Enhances Docosahexaenoic Acid-Induced Apoptosis in Vitro in Lung Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2683
Author(s):  
Rosemary A. Poku ◽  
Kylee J. Jones ◽  
Megan Van Baren ◽  
Jamie K. Alan ◽  
Felix Amissah
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Molecular Mechanisms ◽  
Cancer Cell Lines ◽  
Soft Agar ◽  
Lung Cancer Cell ◽  
Anticancer Activities ◽  
The Impact

Polyunsaturated fatty acids (PUFAs) and non-steroidal anti-inflammatory drugs (NSAIDs) show anticancer activities through diverse molecular mechanisms. However, the anticancer capacities of either PUFAs or NSAIDs alone is limited. We examined whether combining NSAIDs with docosahexaenoic (DHA), commonly derived from fish oils, would possibly synergize their anticancer activity. We determined the viability of lung cancer cell lines (NCI-H1573, A549, NCI-H1299, and NCI-H1975) after exposure to DHA and various NSAIDs. We further conducted cell apoptosis assays and analyzed apoptosis-associated proteins and some key proteins in the RAS/MEK/ERK and PI3K/Akt pathways using western blot analysis. We also determined the impact of the treatment on the expression of inducible cancer-related genes using nCounter PanCancer Pathways gene expression analysis. The results showed that the combination of DHA and NSAIDs increased suppression of cell viability in all the lung cancer cell lines tested compared to each of the compounds used alone, with diclofenac being the most potent NSAID tested. This synergistic effect is especially significant in A549 and NCI-H1573 cells. The combination treatment was more effective at inhibiting clonogenic cell growth and anchorage-independent growth in soft agar, inducing caspase-dependent apoptosis, and altering expression of critical proteins in the RAS/MEK/ERK and PI3K/Akt pathways. The data from this study demonstrate that DHA combined with low dose diclofenac provides greater anticancer potential, which can be further developed for chemoprevention and adjunct therapy in lung cancer.

scholarly journals Expression profiling of lung cancer cell lines

10.1038/87074 ◽  
2001 ◽  
Vol 27 (S4) ◽  
pp. 53-53
Author(s):  
Priya Dayananth ◽  
Terri McClanahan ◽  
Ferdous Gheyas ◽  
Marco Hernandez ◽  
Wei Ding ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Expression Profiling ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell

scholarly journals Failure of apoptosis and activation on NFκB by celecoxib and aspirin in lung cancer cell lines

2007 ◽  
Author(s):  
Angela Gradilone ◽  
Ida Silvestri ◽  
Susanna Scarpa ◽  
Stefania Morrone ◽  
Orietta Gandini ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Lung Cancer Cell

scholarly journals Cancer stem cells and cisplatin‐resistant cells isolated from non‐small‐lung cancer cell lines constitute related cell populations

2014 ◽  
Vol 3 (5) ◽  
pp. 1099-1111 ◽  
Author(s):  
Blanca D. Lopez‐Ayllon ◽  
Veronica Moncho‐Amor ◽  
Ander Abarrategi ◽  
Inmaculada Ibañez Cáceres ◽  
Javier Castro‐Carpeño ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cell Populations ◽  
Lung Cancer Cell ◽  
Related Cell ◽  
Resistant Cells
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