Project description:Purpose: Analysis of the regulatory network involved in DSTY in lung cancer cells. Methods: mRNA profiles of A549 knockdown cell group and A549 NC group were generated by deep sequencing, using Illumina Novaseq platform. Index of the reference genome was built using Hisat2 v2.0.5 and paired-end clean reads were aligned to the reference genome using Hisat2 v2.0.5. featureCounts v1.5.0-p3 was used to count the reads numbers mapped to each gene. And then FPKM of each gene was calculated based on the length of the gene and reads count mapped to this gene. Differential expression analysis of two conditions/groups (two biological replicates per condition) was performed using the DESeq2 R package (1.16.1). The resulting P-values were adjusted using the Benjamini and Hochberg’s approach for controlling the false discovery rate .Genes with an adjusted P-value <0.05 found by DESeq2 were assigned as differentially expressed. Clusterprofiler software was used to perform GO function enrichment analysis and KEGG pathway enrichment analysis of the differential gene sets. Results: We identified 2555 differential genes, of which 1444 were up-regulated and 1111 were down-regulated in A549 sh1 VS NC. In GO enrichment analysis,the biological process is mainly in the cell ions homeostasis and the molecular function is mainly in inflammation response,chemotaxis,innate immune response, and extracellular matrix. KEGG analysis shows that differential genes are enriched in cytokine-cytokine receptor interaction ,JAK-STAT signaling pathway and PI3K-Akt signaling pathways.We identified 2600 differential genes, of which 1523 were up-regulated and 1077 were down-regulated in A549 sh4 VS NC. In GO enrichment analysis,the biological process is mainly in the cell ions homeostasis and the molecular function is mainly in chemokine receptor binding,nic hydroxy compound metabolic process,alcohol metabolic process, and extracellular matrix. KEGG analysis shows that differential genes are enriched in cytokine-cytokine receptor interaction ,glutathione metabolism and chemical carcinogenesis. Conclusion: Based on RNA-seq analysis, the regulatory network involved in DSTY in Lung cancer .
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.
Project description:In this study, we explored the role of FXR in the response to ionizing radiation (IR) in A549 human lung cancer cells. FXR was stably knocked down in A549 cells using shRNA, and four experimental groups were established: control A549 cells (non-irradiated), control A549 cells (irradiated), FXR knockdown A549 cells (non-irradiated), and FXR knockdown A549 cells (irradiated). RNA sequencing (RNA-seq) was performed to identify gene expression changes associated with FXR knockdown and irradiation. This dataset provides insights into the molecular mechanisms by which FXR influences the cellular response to radiation and its potential impact on cancer therapy.