scholarly journals Tumor-suppressive effect of LRIG1, a negative regulator of ErbB, in non-small cell lung cancer harboring mutant EGFR

2018 ◽  
Vol 39 (5) ◽  
pp. 719-727 ◽  
Author(s):  
Hidejiro Torigoe ◽  
Hiromasa Yamamoto ◽  
Masakiyo Sakaguchi ◽  
Chen Youyi ◽  
Kei Namba ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Suppressive Effect ◽  
Small Cell ◽  
Negative Regulator ◽  
Small Cell Lung ◽  
Tumor Suppressive Effect ◽  
Mutant Egfr

scholarly journals Targeting the Oncogenic MUC1-C Protein Inhibits Mutant EGFR-Mediated Signaling and Survival in Non–Small Cell Lung Cancer Cells

2014 ◽  
Vol 20 (21) ◽  
pp. 5423-5434 ◽  
Author(s):  
Akriti Kharbanda ◽  
Hasan Rajabi ◽  
Caining Jin ◽  
Jeremy Tchaicha ◽  
Eiki Kikuchi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
C Protein ◽  
Mutant Egfr

scholarly journals The Inhibitory Mechanisms of Tumor PD-L1 Expression by Natural Bioactive Gallic Acid in Non-Small-Cell Lung Cancer (NSCLC) Cells

Cancers ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 727 ◽  
Author(s):  
Dong Young Kang ◽  
Nipin Sp ◽  
Eun Seong Jo ◽  
Alexis Rugamba ◽  
Dae Young Hong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Gallic Acid ◽  
Cell Lung Cancer ◽  
Growth Factor Receptor ◽  
Suppressive Effect ◽  
Small Cell ◽  
Small Cell Lung ◽  
Peripheral Blood Mononuclear ◽  
Akt Phosphorylation

Non-small-cell lung cancer (NSCLC) is the most common lung cancer subtype and accounts for more than 80% of all lung cancer cases. Epidermal growth factor receptor (EGFR) phosphorylation by binding growth factors such as EGF activates downstream prooncogenic signaling pathways including KRAS-ERK, JAK-STAT, and PI3K-AKT. These pathways promote the tumor progression of NSCLC by inducing uncontrolled cell cycle, proliferation, migration, and programmed death-ligand 1 (PD-L1) expression. New cytotoxic drugs have facilitated considerable progress in NSCLC treatment, but side effects are still a significant cause of mortality. Gallic acid (3,4,5-trihydroxybenzoic acid; GA) is a phenolic natural compound, isolated from plant derivatives, that has been reported to show anticancer effects. We demonstrated the tumor-suppressive effect of GA, which induced the decrease of PD-L1 expression through binding to EGFR in NSCLC. This binding inhibited the phosphorylation of EGFR, subsequently inducing the inhibition of PI3K and AKT phosphorylation, which triggered the activation of p53. The p53-dependent upregulation of miR-34a induced PD-L1 downregulation. Further, we revealed the combination effect of GA and anti-PD-1 monoclonal antibody in an NSCLC-cell and peripheral blood mononuclear–cell coculture system. We propose a novel therapeutic application of GA for immunotherapy and chemotherapy in NSCLC.

scholarly journals A case treated with nivolumab after small cell lung cancer transformation of mutant EGFR non-small cell lung cancer

2016 ◽  
Vol 27 (12) ◽  
pp. 2300-2301 ◽  
Author(s):  
S. Nishikawa ◽  
Y. Tambo ◽  
H. Ninomiya ◽  
T. Oguri ◽  
Y. Kawashima ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Mutant Egfr

Molecular abnormalities in lung cancer.

1998 ◽  
Vol 16 (3) ◽  
pp. 1207-1217 ◽  
Author(s):  
R Salgia ◽  
A T Skarin
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Molecular Mechanisms ◽  
Cellular Proliferation ◽  
Small Cell ◽  
Negative Regulator ◽  
Small Cell Lung ◽  
Molecular Abnormalities

PURPOSE To review several recently described molecular abnormalities in lung cancer and discuss their potential diagnostic and therapeutic relevance. DESIGN Articles were identified through a Medline search (1966 to 1997) and studies, including reviews, were cited in the references. RESULTS Molecular mechanisms altered in lung cancer include induced expression of oncogenes, such as RAS, MYC, c-erbB-2, and BCL-2, and loss of tumor-suppressor genes, such as RB, p53, and p16INK4A. RAS is a 21-kd G protein and up to 30% of adenocarcinomas show mutations in K-RAS oncogene. MYC encodes a transcriptional activator and amplification may adversely affect survival in small-cell lung cancer (SCLC). The growth factor receptor c-erbB-2 is overexpressed in up to 25% of non-small-cell lung cancer (NSCLC) cases. BCL-2, a negative regulator of apoptosis, is expressed differently in some NSCLCs. Abnormalities of RB, a key regulator of cell cycle, are detected in greater than 90% of SCLCs. There is an inverse relationship in lung cancer cells between expression of RB and p16INK4A, an upstream regulator of RB. Mutations of p53, with frequencies up to 50% in NSCLC and 80% in SCLC, can lead to loss of tumor-suppressor function, cellular proliferation, and inhibition of apoptosis. The identified molecular abnormalities in lung cancer are currently used to develop diagnostics for detecting early disease, as well as to identify targets for gene therapy. CONCLUSION Genetic abnormalities involved in the pathogenesis of lung cancer are rapidly being delineated. Understanding molecular abnormalities in lung cancer could potentially lead to earlier diagnosis and the development of novel investigational approaches to the treatment of lung cancer.

scholarly journals Association between microRNA-146a, -499a and -196a-2 SNPs and non-small cell lung cancer: a case–control study involving 2249 subjects

2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Hao Qiu ◽  
Zhiqiang Xie ◽  
Weifeng Tang ◽  
Chao Liu ◽  
Yafeng Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Case Control Study ◽  
Case Control ◽  
Small Cell ◽  
Negative Regulator ◽  
Value Assessment ◽  
Small Cell Lung ◽  
Control Study

Abstract MicroRNA (miR) acts as a negative regulator of gene expression. Many literatures have suggested that miRs may be involved in the process of cell proliferation, inflammation, oxidative stress, energy metabolism and epithelial–mesenchymal transition. Thus, miRs may be implicated in the occurrence of non-small cell lung cancer (NSCLC). In the current investigation, we included 2249 subjects (1193 NSCLC patients and 1056 controls) and designed a study to identify the relationship of miR-146a rs2910164 C/G, -499a rs3746444 A/G and -196a-2 rs11614913 T/C with the risk of NSCLC. The risk factors (e.g., body mass index (BMI), sex, smoking, drinking and age) was used to adjust the odds ratios (ORs) and 95% confidence intervals (CIs). After conducting a power value assessment, we did not confirm that the miR-single nucleotide polymorphisms (SNPs) genotypic distributions were different in NSCLC cases and controls. However, the association of miR-196a-2 rs11614913 with a decreased risk of NSCLC was identified in the female subgroup (adjusted P=0.005, power = 0.809 for TC vs. TT, and adjusted P=0.004, power = 0.849 for CC/TC vs. TT). In addition, gene–gene interaction analysis showed that rs11614913 TC/3746444 AA and rs11614913 CC/rs3746444 AA could also reduce the susceptibility to NSCLC (rs11614913 TC/rs3746444 AA vs. rs11614913 TT/rs3746444 AA, P=0.001, power = 0.912 and rs11614913 CC/rs3746444 AA vs. rs11614913 TT/rs3746444 AA, P=0.003, power = 0.836). In conclusion, in overall comparisons, we did not confirm that the rs2910164, rs3746444, and rs11614913 SNPs genotypic distributions were different in NSCLC cases and controls. However, this case–control study demonstrates that miR-196a-2 rs11614913 may be a protective factor for the development of NSCLC among female patients.

scholarly journals HSP70 Causes EGFR-Tkis Resistance in a Mutant EGFR Expressed Non-Small-Cell Lung Cancer

2012 ◽  
Vol 23 ◽  
pp. xi116
Author(s):  
T. Ohmori ◽  
T. Yamaoka ◽  
Y. Ichihashi ◽  
T. Hirose ◽  
N. Saijo
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Egfr Tkis ◽  
Mutant Egfr
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