Project description:Lung cancer is one of the most common cancers in the world, which accounts for about 27% of all cancer deaths. However, the mechanisms underlying the pathogenesis of lung cancer cells remain largely elusive. In this study, we examined the role of the Forkhead box protein P1 (FOXP1) in lung cancer development. Our Oncomine analysis shows that FOXP1 is downregulated in lung adenocarcinoma compared with normal lung tissue. Knockdown of FOXP1 promotes the proliferation growth and invasion of PC9 and A549 cells by regulating genes of chemokine signaling molecules, including CCR1, ADCY5, GNG7, VAV3, and PLCB1. Simultaneous knockdown of CCR1 and FOXP1 attenuated FOXP1 knockdown-induced increase of lung cancer cell growth. Finally, knockdown of FOXP1 in PC9 cells promotes the tumorigenesis via CCR1 signaling in xenograft mouse model. Taken together, our data suggest that FOXP1 plays important roles in preventing lung adenocarcinoma development via suppressing chemokine signaling pathways. Novel strategies might be developed to prevent the development of lung adenocarcinoma by targeting FOXP1

2018-02-10 | GSE108500 | GEO

Gene expression of PC9 and PC9-OR cell line [JXQ_RNA]

Project description:To investigate the abnormal gene expression in Osimertinib Resistance lung cancer cell line, We performed gene expression profiling analysis using data obtained from RNA-seq of PC9 cell line and PC9-OR cell line.

2024-03-13 | GSE222820 | GEO

IL-8 Confers Acquired Resistance to EGFR Inhibitors through Regulating Stem Cell-like Properties in Lung Cancer

Project description:Previous study has demonstrated that PC9/gef cells are resistant to gefitinib-induced aspoptosis. To investigate the regulators contributed to gefitinib resistance in lung cancer, we analyzed the gene expression profiles between PC9 and PC9/gef cells. Our results showed that IL-8 contributes to gefitinib resistance and cancer stemness. In contrast, IL-8 knockdown decreased stem-like characteristics and increased gefitinib-induced apoptosis in PC9/gef cells. RNAs extracted from gefitinib-sensitive PC9 cells and gefitinib-resistant PC9/gef cells were hybridized on Affymetrix microarrays. We tried to compare the differential gene expression profiles between PC9 and PC9/gef cells to identify the possible regulators in gefitinib resistance.

2015-08-12 | E-GEOD-60189 | biostudies-arrayexpress

Gene expression profiling of drug-tolerant persister PC9 non-small cell lung cancer cells derived from osimertinib treatment

Project description:Targeting drug tolerant persister (DTP) cells may present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. We sought to identify therapeutically exploitable vulnerabilities in DTP cells using the EGFR-mutant non-small cell lung cancer cell line PC9 as an experimental model. Here we provide RNAseq gene expression profiling data generated from parental PC9 cells compared to PC9 DTP cells generated from nine days of treatment with 2 uM osimertinib. These data can be used to identify genes and pathways which are upregulated in DTP cells, revealing potential therapeutic targets.

2020-06-25 | GSE153183 | GEO

IL-8 Confers Acquired Resistance to EGFR Inhibitors through Regulating Stem Cell-like Properties in Lung Cancer

2015-08-12 | GSE60189 | GEO

Transcriptome analysis of PC9 cells with gefitinib or/and hypoxia treatment and comparison with gefitinib resistant PC9 cells and ALDH positive PC9 cells

Project description:Inevitable gefitinib resistance and relapse of the disease was the biggest hurdle to NSCLC treatment. Importantly, the role of hypoxia in solid tumor tissues in vivo in gefitinib acquired resistance and its relationship to lung cancer stem cells (LCSCs) has not been fully elucidated. Here, the PC9 cells were treated with short term gefitinib or/and hypoxia, also, PC9 gefitnib resistant (PC9-GR) cell line was established and ALDH positive PC9 cells were sorted by FACs. Transcriptome analysis among those PC9 cell groups revealed the important role of hypoxia in gefitinib acquired resistance and signaling transduction change, which may critical for NSCLC disease progression and recurrence.

2017-10-31 | GSE69599 | GEO

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