Project description:We depleted TIMM13 using short interfering RNA (siRNA) in A549 lung cancer cells, and found that silencing of TIMM13 could significantly inhibit A549 cell proliferation. Thus, we conducted RNA-seq in the A549 cells transduced with either nontargeting siRNA or two distinct TIMM13-specific siRNAs. We observed widespread gene expression change in A549 cells upon TIMM13 knockdown.
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of wild type and MYOCD Knockdown in human lung cancer cell line A549. Methods: mRNA profiles of wild type(WT) and Dox inducible MYOCD Knockdown (MYOCD−/−) human lung cancer cell line A549 were generated by deep sequencing, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR.
Project description:The human lung cancer cell line A549 with high CD43 expression was stably trasfected with a vector expressing a non-functional shRNA or 3 of these same vectors each expressing a different shRNA targeting human CD43 mRNA. The transcriptomes of these two daughter lines were then compared by differential microarray analysis. The generation and functional characteristics of these two daughter cell lines are described by Fu et al., in the International Journal of Cancer, volume 132, pages 1761-1770, published in 2013.
Project description:NEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human lung cancer cell line A549, which has LKB1 loss-of-function mutation and increased expression of NEDD9, was used for two individual NEDD9 knockdown. Human lung cancer cell line CRL-5907, which has wild-type LKB1 and low NEDD9 expression level, was used for NEDD9 overexpression. The microarray was done in A549 cells, A549 cells with two different NEDD9 knockdown; CRL-5907 cells and CRL-5907 cells with NEDD9 overexpression.
Project description:Nicotine and nicotinic acetylcholine receptors (nAChRs) are considred to be involved in the progression of lung carcinomas. α5-nAChR is believed to be associated with lung cancer risk and onset, however its function and physiologic roles is far from clear. We use microarry to detail the global programme of gene expression underlying knockdown CHRNA5, encoding α5-nAChR, in human lung cancer A549 cells compared with control.
Project description:HSPD1 knockdown was established in A549 cells using an shRNA approach. Secretomes from both shHSPD1-A549 and shControl-A549 cells were collected and subjected to label-free comparative proteome analysis using SWATH-MS.