Project description:A lung cancer cell model of invasive transformation was developed to select progressively invasive cell populations from a parental cell line of human lung adenocarcinoma, CL1. Five progressive sub-clones namely, CL1-1, CL1-2, CL1-3 CL1-4, and CL1-5 were selected using transwell and displayed increasing invasion potential (Chu et al, 1997). Here, we used microarrays to analyze and compare gene expression profiles between CL1-0 and CL1-5 for the identification of invasion/metastasis associated gene signatures.
Project description:A lung cancer cell model of invasive transformation was developed to select progressively invasive cell populations from a parental cell line of human lung adenocarcinoma, CL1. Five progressive sub-clones namely, CL1-1, CL1-2, CL1-3 CL1-4, and CL1-5 were selected using transwell and displayed increasing invasion potential (Chu et al, 1997). Here, we used microarrays to analyze and compare gene expression profiles between CL1-0 and CL1-5 for the identification of invasion/metastasis associated gene signatures. CL1-0 and CL1-5 lung cancer cell lines were used for RNA extraction and hybridization on Affymetrix microarrays. A total of 6 chips were used for microarray analysis including three biological repeats from CL1-0 and three biological repeats from CL1-5.
Project description:Highly metastatic cancer cells have been observed to move directionally in response to direct current (dc) electric fields (EFs) of physiological strength. The phenomenon, which is called electrotaxis or galvanotaxis, suggests the involvement of physiological EF in cancer metastasis. To explore this conjecture, we compared the influence of dcEF on gene expressions of a highly invasive (CL1-5) and a low invasive (CL1-0) lung cancer cell lines. Gene expression of human lung cancer cells with (experimental samples) or without (control samples) dcEF stimulation in physiological strength was analyzed. Two cell lines, CL1-0 and CL1-5, were treated with the same condition and compared in this study. Each condition has three biological replicates for each cell line.
Project description:Purpose: Epigenetic drug DNA methyltransferase inhibitors (DNMTis) are immunomodulating agents that may sensitize cancer cells to immune cell attack. However, it is still unclear how DNMTi affects cancer cells to the killing by immune cells. We therefore try to uncover the alternations of genomic DNA methylation after DNMTi treatment of cancer cells. Methods: Six human lung cancer cell lines (A549, H1299, CL1-0, CL1-5, H1792, PC9) before (Mock) and after (DAC) treatement with 100 nM decitabine (DAC) for 72 hours followed by growing in drug-free medium for three days were subjected to Illumina MethylationEPIC microarray analysis. Results: DNA methylome analysis reveals DNMTi-induced DNA demethylation at transcription start site (TSS)-flanking regions of several actin, intermediate filament and microtubule molecules in human lung cancer cell lines. Conclusion: Decitabine primes lung cancer cells to γδ T cell-mediated killing through regulating cytoskeleton associated genes potentially involved in immune synapse formation.
Project description:Purpose: Epigenetic drug DNA methyltransferase inhibitors (DNMTis) are immunomodulating agents that may sensitize cancer cells to immune cell attack. However, it is still unclear how DNMTi affects cancer cells to the killing by immune cells. We therefore try to uncover the alternations of genomic DNA methylation, chromatin accessibility and transcriptomes after DNMTi treatment of cancer cells. Methods: Six human lung cancer cell lines (A549, H1299, CL1-0, CL1-5, H1792, PC9) treated without (Mock) or with 100 nM decitabine (DAC) for 72 hours followed by growing in drug-free medium for three days were subjected to mRNA-seq and Omni-ATAC-seq analyses. Results: mRNA-seq and ATAC-seq analyses reveal upregulation of actin and intermediate filament, and downregulation of microtubule modules by decitabine in human lung cancer cell lines. Conclusion: Decitabine primes lung cancer cells to γδ T cell-mediated killing through regulating cytoskeleton associated genes potentially involved in immune synapse formation.