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: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: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.
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.
2013-01-15 | GSE43249 | GEO
Project description:Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line
Project description:The cellular transcriptome of untreated and cisplatin-treated A549 non-small cell lung cancer cells and their cisplatin-resistant sub-line A549rCDDP2000 was screened with a whole genome array for gene candidates relevant for cisplatin resistance.
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:Combination therapy as an important treatment option for lung cancer has been attracting attention due to the primary and acquired resistance of chemotherapeutic drugs in the clinical application. In the present study, as a new therapy strategy, concomitant treatment with time-restricted feeding (TRF) plus cisplatin (DDP) on lung cancer growth was investigated in DDP-resistant and DDP-sensitive lung cancer cells. We first found that TRF significantly enhanced the drug susceptibility of DDP in DDP-resistant A549 (A549/DDP) cell line, illustrated by reversing the inhibitory concentration 50 (IC50) values of A549/DDP cells to normal level of parental A549 cells. We also found that TRF markedly enhanced DDP inhibition on cell proliferation, migration, as well as promoted apoptosis compared to the DDP-alone group in A549, H460 and A549/DDP cells lines. We further revealed that the synergistic anti-tumor effect of combined DDP and TRF was greater than that of combined DDP and simulated fasting condition (STS), a known anti-tumor cellular medium. Moreover, mRNA sequence analysis from A549/DDP cell line demonstrated the synergistic anti-tumor effect involved in upregulated pathways in p53 signaling pathway and apoptosis. Notably, compared with the DDP-alone group, combination of TRF and DDP robustly upregulated the P53 protein expression without mRNA level change by regulating its stability via promoting protein synthesis and inhibiting degradation, revealed by cycloheximide and MG132 experiments. Collectively, our results suggested that TRF in combination with cisplatin might be an additional novel therapeutic strategy for patients with lung cancer
Project description:Long noncoding RNAs are newly discovered regulators that play a critical role in cell biology, crucial to the correct functioning of the cell. Alterations in lncRNAs can lead to the development of diseases such as cancer. However, the role of lncRNAs in resistance to platinum chemotherapy is largely unknown. To screen for epigenetic changes involved in the development of resistance, we combined lncRNA and mRNA expression microarrays with whole genome bisulfite sequencing (WGBS) in four paired cisplatin-sensitive/resistant cells from non-small cell lung cancer and ovarian cancer. We found low levels of expression changes in lncRNAs (1.5%) and mRNAs (2%) when comparing resistant vs. sensitive cells. The correlation between lncRNA/mRNA arrays and WGBS identified two groups of lncRNAs, classified according to their relationship with the gene they have in silico complementarity or with their possible epigenetic regulation at the DNA methylation level. Validation of the results of expression and methylation levels allowed us to characterize lncRNAs in cisplatin-resistant phenotypes. In this study, we characterized lncRNAs that change in cisplatin-resistant cells due to epigenetic regulation at the DNA methylation level and the associated changes in expression levels. We have identified two groups of differentially expressed and methylated lncRNAs, indicating a new approach to the study of the mechanisms involved in the development of acquired resistance to cisplatin in cancer cells.
