Here, we describe a pro-oxidative model in a single human lung carcinomaSPC-A-1 cell that was created by application of extracellular H<sub>2</sub>O<sub>2</sub> stimuli.
Finally, the overexpression and inhibition of FAM98A was performed in the A549 and SPC-A1 cell lines to explore its role in the development of lung cancer.
We also found that knockdown of SOX12 in SPC-A-1 and A549 cells impaired lung cancer cell proliferation, migration and invasion <i>in vitro</i>, but promoted lung cancer cell apoptosis.
Additionally, the new synthesized compounds were evaluated to identify the molecular characteristics that contribute to their cytotoxicity, which was tested against SK-LU-1, SPC-A-1 and 95D human lung cancer cell lines, using the MTT assay.
The expression of TRAF6 was determined in human lung adenocarcinoma A549, non-small cell lung cancer H1650, human airway epithelial Calu-3 and human lung cancerSPC-A1 cell lines using quantitative RT-PCR (qRT‑PCR) and western blotting at the transcriptional and translational levels.
Signal Transducer and Activator of Transcription 1 (STAT1) or a modified STAT1 (designated STAT1-CC) that is hyper-responsive to IFN were overexpressed in lung cancerSPC-A-1 and H1299 cells using lentiviral vectors.
When the chimeric ubiquitin ligases were introduced into lung cancerSPC-A1 cells, they effectively associated with EGFR, promoted its ubiquitination and degradation, and as a result, blocked the downstream PI3K-Akt signal pathway.
We performed methyl thiazolyl tetrazolium and colony formation assays to study the influence of miR-182 on proliferation of the lung cancer cell lines A549 and SPC-A-1.
In this study, bisulfite sequencing PCR showed that the β-catenin promoter region in SPC-A-1 and LTEP-a-2 lung cancer cell lines has Kaiso binding sites sequences and CpG islands which may combine with Kaiso.
Through si-RNA-mediated functional screens, Myosin heavy chain 9 (MYH9) and Copine III (CPNE3) were indicated as positively correlating with the migration and invasion properties of SPC-A1sci cells, and the same function of CPNE3 was confirmed in another lung cancer cell line, H1299.
To identify the key regulatory genes involved in lung cancer, we performed a combination of gene array and bioinformatics analyses to compare gene transcription profiles in 3 monoclonal cell strains with high, medium or low metastatic abilities, which were separated from the SPC-A-1sci and SPC-A-1 cell lines by limiting dilution monoclone assay.
The expression levels of ER (ER-α and ER-β) in lung cancer cell lines (A549, H460, SPC-A-1, H1299) and normal bronchus epithelial cell BEAS-2B were detected using real-time PCR and Western blot.
In our study, the lung cancer cell lines (NCI-H446 and SPC-A-1) displayed numerous numerical and structural alterations in their chromosomes by G-banded karyotypic analysis, and abnormalities of chromosome 12 by fluorescence in situ hybridization.
The results demonstrated the vehicle was able to transfer reporter genes specifically into lung cancerSPC-A1 cells and SPC-A1 xenografts highly expressing Tie2 and epithelial cells of bronchus, but not in heart, liver, spleen, kidney, lung alveolar and vascular tissues.
Here, we examined the effects of the CM from human lung carcinoma cell lines A549 and SPC-A-1 on cultures of primary human umbilical veins endothelial cells (HUVECs).
Gambogic acid inhibits proliferation of human lung carcinomaSPC-A1 cells in vivo and in vitro and represses telomerase activity and telomerase reverse transcriptase mRNA expression in the cells.