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Lentiviral shRNA knockdown of PTK7 in lung adenocarcinoma cell lines NCI-H1299 and NCI-H2009

ABSTRACT: PTK7 was identified from a meta-analysis of 1905 non-small-cell lung cancer (NSCLC) samples across 12 datasets to be one of seven genes commonly up-regulated in lung adenocarcinoma (ADC). Using ADC cell lines NCI-H1299 and NCI-H2009, disruption of PTK7 resulted in decreased cell viability and induction of apoptosis. A xenotransplantation model of the cell lines with PTK7 knock-down also resulted in decreased tumor burden. We assayed gene expression in these cell lines after PTK7 knock-down by shRNA to uncover deregulated pathways and genes. 8 samples were analyzed. In each cell line, we knocked down PTK7 with 2 independent hairpins, and 2 control hairpins targeting luciferase and GFP. Thus, NCI-H1299 has 2 samples of PTK7 knock-down, and 2 samples of control knock down. NCI-H2009 has similar samples.

ORGANISM(S): Homo sapiens

SUBMITTER: Vaka Dedeepya

PROVIDER: S-ECPF-GEOD-50138 | biostudies-other |

REPOSITORIES: biostudies-other

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Lentiviral shRNA knockdown of PTK7 in lung adenocarcinoma cell lines NCI-H1299 and NCI-H2009

Project description:PTK7 was identified from a meta-analysis of 1905 non-small-cell lung cancer (NSCLC) samples across 12 datasets to be one of seven genes commonly up-regulated in lung adenocarcinoma (ADC). Using ADC cell lines NCI-H1299 and NCI-H2009, disruption of PTK7 resulted in decreased cell viability and induction of apoptosis. A xenotransplantation model of the cell lines with PTK7 knock-down also resulted in decreased tumor burden. We assayed gene expression in these cell lines after PTK7 knock-down by shRNA to uncover deregulated pathways and genes. 8 samples were analyzed. In each cell line, we knocked down PTK7 with 2 independent hairpins, and 2 control hairpins targeting luciferase and GFP. Thus, NCI-H1299 has 2 samples of PTK7 knock-down, and 2 samples of control knock down. NCI-H2009 has similar samples.

2014-01-01 | E-GEOD-50138 | biostudies-arrayexpress

Lentiviral shRNA knockdown of PTK7 in lung adenocarcinoma cell lines NCI-H1299 and NCI-H2009

2014-01-01 | GSE50138 | GEO

Human lung cancer cell lines DMS-273 (SCLC) and NCI-H1437 (NSCLC): scrambled vs. shRNA clones

Project description:Transcriptional profiling of two human lung cancer cell lines, DMS-273 (small cell lung cancer) and NCI-H1437 (non-small cell lung cancer), stably transfected either with innocuous scrambled shRNAs or SETDB1-specific.The objective was to identify global gene expression changes due to the depletion of the H3K9me3 methyltransferase SETDB1. 3 replicates for DMS-273 and 1 Control; 2 replicates for NCI-H1437 and 1 Control

| S-ECPF-GEOD-45175 | biostudies-other

Knockdown LRRK1-CAPT in NCI-H1299 lung cancer cell line

Project description:Knockdown LRRK1-CAPT in NCI-H1299 lung cancer cell line by two independent siRNAs, to investigate the mechanism of LRRK1-CAPT in regulation of cell proliferation.

2022-12-18 | GSE220952 | GEO

Transcriptome Analysis of the Inhibitory Effects of 20(S)-Protopanaxadiol on NCI-H1299 Non-Small Cell Lung Cancer Cells.

Project description:Lung cancer seriously threatens human health. To explore the molecular mechanism of 20(S)-Protopanaxadiol (PPD) on human non-small cell lung cancer cells, we investigated the transcriptional profile of PPD-treated NCI-H1299 cells. Cell proliferation, cell cycle, and apoptosis were detected using cell counting kit-8 and flow cytometry, respectively. Differentially expressed genes (DEGs) between PPD-treated and untreated cells were determined using RNA sequencing and bioinformatic analysis. Protein phosphorylation was detected using Western blotting. Data of mRNA expression profiles of lung cancer were from The Cancer Genome Atlas (TCGA) and analyzed using R software version 4.3.1. PPD showed an inhibitory effect on the proliferation of NCI-H1299 cells and induced apoptosis. There were 938 upregulated genes and 466 downregulated genes in PPD-treated cells, and DEGs were primarily enriched in the MAPK signaling pathway. The detection of phosphorylation revealed that the phosphorylation of ERK and p38 MAPK was significantly reduced in PPD-treated cells. Further comparison of PPD-regulated DEGs with clinical data of lung adenocarcinoma demonstrated that most downregulated genes in tumor tissues were upregulated in PPD-treated cells or vice versa. Two PPD-downregulated genes HSPA2 and EFNA2 were associated with patients' overall survival. Therefore, PPD could inhibit NCI-H1299 cells by affecting gene expression and regulating ERK and p38 MAPK pathways.

| S-EPMC10421167 | biostudies-literature

Knockdown LRRK1-CAPT in NCI-H1299 lung cancer cell line

Project description:Knockdown LRRK1-CAPT in NCI-H1299 lung cancer cell line

| PRJNA912146 | ENA

Induction of fetal hemoglobin: Lentiviral shRNA knockdown of HBS1L in β0-thalassemia/HbE erythroid cells.

Project description:Imbalanced globin chain output contributes to thalassemia pathophysiology. Hence, induction of fetal hemoglobin in β-thalassemia and other β-hemoglobinopathies are of continuing interest for therapeutic approaches. Genome-wide association studies have identified three common genetic loci: namely β-globin (HBB), an intergenic region between MYB and HBS1L, and BCL11A underlying quantitative fetal hemoglobin production. Here, we report that knockdown of HBS1L (all known variants) using shRNA in early erythroblast obtained from β0-thalassemia/HbE patients triggers an upregulation of γ-globin mRNA 1.69 folds. There is modest perturbation of red cell differentiation assessed by flow cytometry and morphology studies. The levels of α- and β-globin mRNAs are relatively unaltered. Knockdown of HBS1L also increases the percentage of fetal hemoglobin around 16.7 folds when compared to non-targeting shRNA. Targeting HBS1L is attractive because of the potent induction of fetal hemoglobin and the modest effect on cell differentiation.

| S-EPMC9994754 | biostudies-literature

p27Kip1 knockdown induces proliferation in the organ of Corti in culture after efficient shRNA lentiviral transduction.

Project description:The cells in the organ of Corti do not exhibit spontaneous cell regeneration; hair cells that die after damage are not replaced. Supporting cells can be induced to transdifferentiate into hair cells, but that would deplete their numbers, therefore impairing epithelium physiology. The loss of p27Kip1 function induces proliferation in the organ of Corti, which raises the possibility to integrate it to the strategies to achieve regeneration. Nevertheless, it is not known if the extent of this proliferative potential, as well as its maintenance in postnatal stages, is compatible with providing a basis for eventual therapeutic manipulation. This is due in part to the limited success of approaches to deliver tools to modify gene expression in the auditory epithelium. We tested the hypothesis that the organ of Corti can undergo significant proliferation when efficient manipulation of the expression of regulators of the cell cycle is achieved. Lentiviral vectors were used to transduce all cochlear cell types, with efficiencies around 4 % for hair cells, 43 % in the overall supporting cell population, and 74 % within lesser epithelial ridge (LER) cells. Expression of short hairpin RNA targeting p27Kip1 encoded by the lentiviral vectors led to measurable proliferation in the organ of Corti and increase in LER cells number but not hair cell regeneration. Our results revalidate the use of lentiviral vectors in the study and in the potential therapeutic approaches for inner ear diseases, as well as demonstrate that efficient manipulation of p27Kip1 is sufficient to induce significant proliferation in the postnatal cochlea.

| S-EPMC3705079 | biostudies-literature

Expression data from NCI-H1299 and NCI-H1299/CDDP cells

Project description:Non-small cell lung cancer (NSCLC) patients are prone to drug resistance during chemotherapy. Therefore, in order to compare the changes in the gene expression profiles of NSCLC cells before and after drug resistance, we constructed cisplatin-resistant cells (NCI-H1299/CDDP), and compared the gene expression profiles with those of the parental NCI-H1299 cells. We used microarrays to study in detail the global gene expression changes before and after drug resistance in NSCLC cells and identified genes that were up- or down-regulated during this process.

2024-01-14 | GSE252795 | GEO

GMDS knockdown impairs cell proliferation and survival in human lung adenocarcinoma.

Project description:BackgroundLung adenocarcinoma is the most common type of lung cancer and one of the most lethal and prevalent cancers. Aberrant glycosylation was common and essential in tumorigenesis, with fucosylation as one of the most common types disrupted in cancers. However, it is still unknown whether genes involved in fucosylation are important for lung adenocarcinoma development and process.MethodsGMDS is involved in cellular fucosylation. Here we examined GMDS expression level at both mRNA and protein level in lung adenocarcinoma. The impact of GMDS knockdown on lung adenocarcinoma in vitro and in vivo was investigated. Transcriptome changes with GMDS knockdown in lung adenocarcinoma cells were also examined to provide insights into related molecular mechanisms.ResultsGMDS expression is significantly upregulated in lung adenocarcinoma at both mRNA and protein levels. Lentivirus-mediated shRNA strategy inhibited GMDS expression efficiently in human lung adenocarcinoma cells A549 and H1299, and GMDS knockdown impaired cell proliferation, colony formation ability, induced cell cycle arrest, and apoptosis in both cell lines. Furthermore, GMDS knockdown inhibited tumorigenesis in a xenograft mice model of lung adenocarcinoma. Microarray analysis explored the GMDS-mediated molecular network and revealed that the CASP8-CDKN1A axis might be critical for lung adenocarcinoma development.ConclusionsThese findings suggest that GMDS upregulation is critical for cell proliferation and survival in human lung adenocarcinoma and might serve as a potential biomarker for lung adenocarcinoma diagnosis and treatment.

| S-EPMC5975429 | biostudies-literature

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