RNAi knock down of ASCL1 in human NCI-H1618 small cell lung cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Jiang T
PROVIDER: S-ECPF-MEXP-1857 | biostudies-other | 2009 Feb
REPOSITORIES: biostudies-other
Similar Datasets
Project description:NCI-H1618 cells treated on d0 and d3 with 25 nM control or ASCL1-targeting siRNA. Biologic triplicate RNA samples harvested at day 5.
2008-11-13 | E-MEXP-1857 | biostudies-arrayexpress
Project description:To elucidate the mechanism of radioresistance in non-small cell lung cancer (NSCLC) cells and to identify key molecules conferring radioresistance, the radioresistant subclone NCI-H520/R, derived from the NCI-H520 NSCLC cell line, was established with eight rounds of sublethal irradiation. The radioresistant features were subsequently assessed using a clonogenic assay, analysis of apoptosis and an MTT assay, the gene expression levels were examined using an Agilent Whole Human Genome 4 x 44 k Oligo microarray and Agilent Human miRCURY(™) LNA array, and confirmed by reverse transcription-quantitative polymerase chain reaction. Pathway analysis and Gene Ontology (GO) analysis were performed to determine the biological functions of the subset of differentially expressed genes. miRNA-mRNA correlation analysis between the expression levels of each miRNA and all its predicted target genes was performed to further understand the radioresistance in the NCI-H520 cells. Following eight rounds of sublethal irradiation, a total of 2,862 mRNAs were significantly differentially expressed in the NCI-H520/R cells, including 893 upregulated genes and 1,969 downregulated genes. A total of 162 upregulated miRNAs and 274 downregulated miRNAs were significantly deregulated in the NCI-H520/R cells. Multiple core regulatory processes and signaling pathways were identified as being of likely relevance to radioresistance in NCI-H520/R cells, including the mitogen-activated protein kinase signaling pathway and neurotrophin signaling pathway. The expression of genes associated with radioresistance reflects the complex biological processes involved in clinical cancer cell eradication and requires further investigation for future enhancement of therapy.
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Project description:Affymetrix Hu133 GeneCHIP Microarray data for Control and c-MYC knock-down (KD) human cancer cell lines. Data related to article 'Novel c-MYC target genes mediate differential effects on cell proliferation and migration', from D. CAPPELLEN et al., EMBO Reports; Note: Samples GSM136093 and GSM136094 (Hela cell line, expt 1) were hybridized and normalized separately from the other 18 Samples. Experiment Overall Design: The cells were harvested 3 days after LacZ (Control) and c-MYC (c-MYC KD) small interfering RNA transfection, and total RNA was used for microarray-based global gene expression profiling.
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Project description:Two-drug combination chemotherapy, often including cisplatin and one other drug, remains the standard of care for patients with advanced non-small cell lung cancer (NSCLC). To improve the treatment of late-stage NSCLC and decrease the toxicity of combination chemotherapy, the search for novel drugs remains vigorous. Ent-11?-hydroxy-15-oxo-kaur-16-en-19-oic acid (5F), a bioactive compound isolated from the herb Pteris semipinnata L., has previously been shown to induce apoptosis and inhibit proliferation in various cancer cells. One outstanding property of 5F is its minimal side effects. In the present study, 5F was combined with cisplatin to treat NCI-H23 cells; proliferation, apoptosis and cell cycle arrest were measured by an MTT assay, Annexin V staining/flow cytometry and propidium iodide staining/flow cytometry, respectively. The messenger RNA levels of ?-catenin, glycogen synthase kinase (GSK)-3?, c-Myc and cyclin D1 were determined by reverse transcription-quantitative polymerase chain reaction, and the protein levels of ?-catenin and GSK-3? were measured by western blot analysis. The results revealed that 5F and cisplatin synergistically induced apoptosis and inhibited cell growth, arrested cell cycles in the G0/G1 phase, downregulated ?-catenin, c-Myc and cyclin D1, and upregulated GSK-3?. These findings merit in vivo studies using animal models of NSCLC to confirm the addition of 5F as a third drug to cisplatin-based combination therapy for late-stage NSCLC.
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Project description:siRNA-mediated inhibition compared to untreated cells and cells transfected with nonsense siRNA. Loss of contact inhibition and anchorage-independent growth are hallmarks of cancer cells. In this context, frequent inactivation of the Hippo pathway and subsequent nuclear enrichment of the transcriptional coactivator yes-associated protein (YAP) uncouple cell proliferation and anti-apoptosis from contact inhibition, associated with uncontrolled tumor growth and tumor cell dissemination. However, general molecular mechanisms of tumor-supporting YAP activity remain unclear. In this study, we show that overexpression and nuclear accumulation of YAP in hepatocytes and hepatocellular carcinoma (HCC) cells leads to an induction of the Notch pathways through transcriptional activation of the Notch ligand jagged-1 (Jag-1). This induction of Jag-1 strictly depends on binding of YAP to TEAD4 and does not rely on WNT/β-catenin pathway activity. Co-activation of YAP, TEAD4, Jag-1, and the Notch target gene Hes-1 was significantly higher in HCC from patients with poor prognosis. High-level expression and nuclear accumulation of YAP correlates with Jag-1/Notch activation not only in human HCC tissues, but also in colon and pancreatic cancer tissues. Thus, our data demonstrate that YAP-driven co-activation of the Jag-1/Notch pathway in part facilitates oncogenic properties of the oncogene YAP not only in HCC but also in different gastrointestinal malignancies. Expression profiling of untreated HCC cell lines (control 1), cells transfected with scrambled/nonsense siRNA (control 2), and after siRNA-mediated YAP inhibition.
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Project description:Luteolin is a falconoid compound, which exhibits anticancer properties, however, its contribution to Sirt1-mediated apoptosis in human non-small cell lung cancer remains to be elucidated. The present study confirmed that the anticancer effect of luteolin on NCI?H460 cells was through Sirt1?mediated apoptosis. The NCI?H460 cells were treated with different concentrations of luteolin, and a 3?(4,5?dimethyl?2?thiazolyl)?2,5?diphnyl?2H?tetrazolium bromide assay, cell cycle analysis and annexin?V/fluorescein isothiocyanate and propidium double staining were performed to assess the apoptotic effect of luteolin. Wound healing and Transwell assays were performed to confirm the inhibition of NCI?H460 cell migration. The protein levels of Sirt1 were knocked down in the NCI?H460 cells using a lentivirus to further investigate the role of this protein, and the expression levels of the apoptotic associated proteins, Bad, Bcl?2, Bax, caspase?3 and Sirt1, were measured using western blotting. The results of the present study demonstrated that luteolin exerted an anticancer effect against NCI?H460 cells through Sirt1?mediated apoptosis and the inhibition of cell migration.
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Project description:Osimertinib (OSI, also known as AZD9291) is the newest FDA-approved epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor for non-small cell lung cancer (NSCLC) patients with EGFR T790M mutation. However, resistance to OSI is likely to progress and the study of potential OSI-resistant mechanisms in advanced is necessary. Here, the OSI-resistant NCI-H1975/OSIR cells were established. After cells developed resistance to OSI, cell proliferation was decreased while cell migration and invasion were increased. The NCI-H1975/OSIR cells exhibited more resistance to gefitinib, erlotinib, afatinib, rociletinib, doxorubicin, and fluorouracil, meanwhile showing higher sensitivity to paclitaxel, when compared with NCI-H1975 cells. In addition, the NCI-H1975/OSIR cells did not display multidrug resistance phenotype. The activation and expression of EGFR were decreased after cells exhibited resistance. Compared with NCI-H1975 cells, the activation of ERK and AKT in NCI-H1975/OSIR cells could not be significantly inhibited by OSI treatment. Navitoclax (ABT-263)-induced cell viability inhibition and apoptosis were more significant in NCI-H1975/OSIR cells than that in NCI-H1975 cells. Moreover, these effects of navitoclax in NCI-H1975/OSIR cells could be reversed by pretreatment of Z-VAD-FMK. Collectively, loss of EGFR could pose as one of the OSI-resistant mechanisms and navitoclax might be the candidate drug for OSI-resistant NSCLC patients.
| S-EPMC5348415 | biostudies-literature
Project description:To study the effect of knocking down wingless-related MMTV integration site 2 (Wnt2) expression by RNAi on the growth and signaling pathways of ex vitro-cultured keloid fibroblasts (KFB).Human KFB were isolated from 10 keloid patient specimens. The KFB cells were then transfected with 4 pairs of small interfering RNA (siRNA) targeting human Wnt2, respectively. Reverse transcriptase-polymerase chain reaction and Western blot analysis were conducted to verify the knock down of Wnt2, and the expression of ?-catenin glycogen synthase kinase-3? (GSK-3?) and cyclin D1 were examined.siRNA Wnt2 transfection (siWnt2) resulted in the significant inhibition of Wnt2 expression at both the mRNA and protein levels. The expression of ?-catenin, GSK-3?, p-GSK-3?, and cyclin D1 at the protein level also decreased in siWnt2 cells. siWnt2 resulted in a substantially slower growth and significant delay in cell doubling time of the KFB cells compared with control groups. Further, the siRNA knock down of GSK-3? and ?-catenin resulted in slower proliferation rates, respectively.Wnt2 siRNA has an inhibitive effect on keloid fibroblast proliferation, which may be a potential therapeutic approach for keloid and other human fibrotic diseases.
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Project description:Aldehyde dehydrogenase isozymes ALDH1A1 and ALDH3A1 are highly expressed in non small cell cell lung cancer. Neither the mechanism nor the biological significance for such over expression have been studied. We used microarrays to analyze changes in A549 lung cancer cell line in which ALDH activity was reduced using lentiviral mediated expression of siRNA against both isozymes (Lenti 1+3) Experiment Overall Design: A549 lung cancer cell lines were transduced with lentiviral vectors containing specific siRNA sequences against ALDH1A1, ALDH3A1, both vectors (Lenti 1+3 cells), and against the green flourescent protein (GFP) gene (GFP cells, used as control).
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Project description:Small RNA expression was analysed in total RNA of HeLa cells treated with siRNA toward Luciferase (negative cotrol) or ADAR1.
2013-05-01 | GSE43167 | GEO