Project description:PPARGC1A oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. We generated gene-expression profile of control and PPARGC1A suppressed A549 cells, a lung adenocarcinoma cell line that expresses moderate levels of PPARGC1A to investigate the role of this gene in lung cancer metastasis.
Project description:Alterations in cellular antigen processing and presenting machinery has gained increased interest as a hallmark of cancer-related inflammation. Growing evidence suggest that proteasome composition and immunoproteasome expression can influence antigen processing. By performing immunopeptidomics on A549 lung adenocarcinoma cell line following depletion of proteasome regulator PSME4 we identified alterations in the antigenic landscape resulting from changes in proteasome processing.
Project description:Alterations in cellular antigen processing and presenting machinery has gained increased interest as a hallmark of cancer-related inflammation. Growing evidence suggest that proteasome composition and immunoproteasome expression can influence antigen processing. By performing immunopeptidomics on A549 lung adenocarcinoma cell line following depletion of proteasome regulator PSME4 we identified alterations in the antigenic landscape resulting from changes in proteasome processing.
Project description:To establish effective multitargeted KRAS pathway therapy, we analyzed mediators of acquired resistance to chronic momelotinib and MEK inhibitor exposure in A549 cells. Since inhibitor resistance was completely reversible after drug withdrawal for several passages, suggesting epigenetic reprogramming, we investigated whole mRNA expression profiles in A549, momelotinib and selumetinib resistant (MSR)-A549 cells and MSR-A549 cells following drug withdrawal for 10 days. In parallel, we also examined mRNA expression profiles of MSR-A549 cells treated with the BET inhibitor JQ1, to identify specific targets regulated by H3K27 acetylation.
Project description:This study aims to identify pathway involvement in the development of cisplatin (cis-diamminedichloroplatinum (II); CDDP) resistance in A549 lung cancer (LC) cells by utilizing advanced bioinformatics software. We developed CDDP-resistant A549 (A549/DDP) cells through prolonged incubation with the drug and performed RNA-seq on RNA extracts to determined differential mRNA and miRNA expression between A549/DDP and A549 cells
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
Project description:Embelin (15 uM) induced alterations in the gene expression profile was studied in A549 lung cancer cells during the initial stages of apoptosis (4h following treatment)
Project description:To identify genes regulated by SPDEF or FOXA3 in A549 lung carcinoma cells, we analyzed the whole-transcriptomic mRNA profiles of A549 cells expressing SPDEF or FOXA3 based on RNA-seq.
Project description:To investigate the difference of miRNA expression between lung cancer cell A549 and its DDP-resistant cell strain A549/DDP, we have employed miRNA microarray expression to discover the difference expression of miRNAs of A549 cells and A549/DDP. We conducted RT-qPCR to examine the expression levels of top differential expressed miRNAs, namely, miR-197-5p, miR-4443, miR-642a-3p, miR-27b-3p and miR-100-5p, confirming low variability between two methods. The A549/DDP was established from A549 in our laboratory, by exposing A549 to gradually increasing DDP concentrations, until the final concentration at 1μg/ml. To avoid the influence of drug to the A549/DDP cells, they were cultured in a drug-free medium for at least two weeks before gene expression analysis. miRNA expression of A549 and A549/DDP was then analzyed.
Project description:This experiment is designed to evaluate gene expression alteration and significant pathway(s) following miR-128 transduction in A549 lung cancer cells. We find several significant pathways, including the Wnt/β-catenin signaling and TGF-β signaling activated by miR-128 overexpression. Total RNA were extracted from A549 lung cancer cells stably transduced with miR-128 precursor or vector control and subjected to mRNA microarray (Agilent-014850 Whole Human Genome Microarray 4x44K) analysis, with two biological replications for each treatment.