The profiles of circRNAs, lncRNAs and mRNAs in drug-resistant non-small-cell lung cancer cell lines by RNA sequencing
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE132418 | GEO | 2020/04/06
REPOSITORIES: GEO
Similar Datasets
Project description:The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs), such as erlotinib. Chromatin-modifying agents offer a novel therapy approach by sensitizing tumor cells to TKIs. The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) and NCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation were quantified by WST-1 assay, apoptosis by Annexin V/7-AAD flow cytometry and histone marks (acH3, H3K4me1,-2,-3) by immunoblotting. Expectedly, the EGFR wt cell lines A549 and NCI-H460 were insensitive to the growth-inhibiting effect of single-agent erlotinib (IC50 70-100µM), compared to HCC827 (IC50 <0.02μM). Treatment with panobinostat diminished growth to <50% in both EGFR wt and <30% in HCC827 cells. The combination of both drugs significantly reduced proliferation by ≥70% in A549, >95% in HCC827, but not further in NCI-H460. Panobinostat alone induced differentiation and expression of p21WAF1/CIP1 and p53 in all three cell lines, with almost no further increase when combined with erlotinib. In contrast, combination treatment additively decreased pERK, pAKT and pEGFR in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we also saw an induction of H3K4 methylation marks in all three cell lines. In conclusion, panobinostat synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in adenocarcinoma EGFR wt patients, combination therapy with an HDACi might offer a promising therapy approach to extend this activity. Copy-number analysis of three NSCLC cell lines HCC827, A549 and NCI-H460 (in unicates) was performed according to protocol by Affymetrix Genome-Wide Human SNP-Array 6.0.
2014-12-03 | E-GEOD-63784 | biostudies-arrayexpress
Project description:The location of nasophryngeal cancer is hidden,so ti is difficult to diagnose at an early stage.In this study,we aimed to investigate expression profiles of circRNAs,mRNAs and IncRNAs and to provide some basis for further study.The expression profiles of circRNAs, mRNAs and lncRNAs were analyzed by microarray technology. The differentially expressed ncRNA was calculated by bioinformatics. Our study characterized the landscape of circRNAs, mRNAs and lncRNAs in NPC tissue and provided novel insights into the molecular mechanisms of NPC.
2023-12-01 | GSE218847 | GEO
Project description:Subcutaneous preadipocyte differentiation play a critical role in fat deposition of pigs. However, the action of different RNAs in subcutaneous preadipocyte differentiation, such as messenger RNAs (mRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), are still largely unclear. In the present study, a transcriptome analysis including mRNAs, lncRNAs, and circRNAs was performed in different stages of D0, D2, D4, and D8 using RNA-seq technology. Our results identified 1,554, 470, 1,344, 1,777, and 676 differentially expressed (DE) mRNAs, 112, 58, 95, 136, and 93 DE lncRNAs, and 902, 787, 710, 932, and 850 DE circRNAs between D2 and D0, between D4 and D2, between D8 and D4, between D4 and D0, and between D8 and D0, respectively. Moreover, functional enrichment analysis showed that the common DE mRNAs during entire differentiation were mainly involved in lipid metabolic and cell differentiation processes. Additionally, co-expression network analysis identified the potential lncRNAs related to adipogenesis, e.g., MSTRG.42239 and MSTRG.146410. Taken together, this study provides a genome-wide landscape of RNA expression profiles during subcutaneous preadipocyte differentiation, thus improving our understanding of molecular mechanism in regulating subcutaneous adipogenesis of pigs.
2018-11-14 | GSE114583 | GEO
Project description:Chemoresistance is a major cause of poor prognosis of breast cancer.More and more mRNAs and lncRNAs are reported to upregulate chemoresistance in breast cancer.To explore the how mRNAs and lncRNAs involved in chemoresistance of breast cancer,we sceened upregulated mRNAs and lncRNA from parental MCF-7 , chemoresistant MCF-7 cells as well as 4 breast cancer tissue sensitive to chemotherapy and 4 resistant to chemotherapy . Total RNA was extracted using Trizol reagent. Agilent Human lncRNA Microarray V6 (4*180K) was used to analyze the global profiling of human lncRNAs and protein-coding transcripts in these samples. The microarray contains 83,835 lncRNAs and 27,233 coding genes.
2020-02-25 | E-MTAB-8787 | biostudies-arrayexpress
Project description:In this study, we established an gefitinib resistant lung adenocarcinoma cell line (i.e. PC9/GR) from lung adenocarcinoma PC9 cell line which was sensitive to gefitinib. Then microarray was performed to elucidate the lncRNAs, cirRNAs and mRNAs involved in gefitinib resistance.
2022-04-11 | GSE169513 | GEO
Project description:Colorectal cancer (CRC) is recognized as the third most common cancer worldwide, and it is one of the leading causes of cancer-related death. However, the current therapeutic regimens were not always effective. Here, the expression profiles of mRNAs, lncRNAs and circRNAs in four pairs of HCT116 and FHC cells were detected by microarray technology
2022-08-18 | GSE211496 | GEO
Project description:In this study, to identify the target genes of PWRN2, we first constructed lentivirus shRNA vectors to infect the KGN cell lines to gain three KGN/shPWRN2 cell lines with down-regulated PWRN2 expression levels. Then, the expression profiles of mRNAs and lncRNAs in KGN/shPWRN2 cells were determined by microarray. The results revealed thousands of lncRNAs and mRNAs expressed in KGN/shPWRN2. The expression of 176 lncRNAs significantly changed in KGN/shPWRN2 cell lines relative to control NC cell lines. Among these, 118 were up-regulated, whereas 58 were down-regulated. A total of 131 mRNAs significantly changed in expression: 84 were upregulated, and 47 were downregulated (fold change≥2.0, P value<0.05). We further do some bioinformatic analysis for the data. Our results will provide some new information to help us understand the molecular roles of PWRN2.
2018-01-01 | GSE97772 | GEO
Project description:Cross-talk between competitive endogenous RNAs (ceRNAs) may play a critical role in revealing potential mechanisms of tumor development and physiology. Glioblastoma is the most common type of malignant primary brain tumor, and the mechanisms of tumor genesis and development in glioblastoma are unclear. Here, to investigate the role of non-coding RNAs and the ceRNA network in glioblastoma, we performed paired-end RNA sequencing and microarray analyses to obtain the expression profiles of mRNAs, lncRNAs circRNAs and miRNAs. We identified that the expression of 501 lncRNAs, 1789 mRNAs, 2038 circRNAs and 143 miRNAs were often altered between glioblastoma and matched normal brain tissue. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed on these differentially expressed mRNAs and miRNA-mediated target genes of lncRNAs and circRNAs. Furthermore, we used a multi-step computational framework and several bioinformatics methods to construct a ceRNA network combining mRNAs, miRNAs, lncRNAs and circRNA, based on co-expression analysis between the differentially expressed RNAs. We identified that plenty of lncRNAs, CircRNAs and their downstream target genes in the ceRNA network are related to glutamatergic synapse, suggesting that glutamate metabolism is involved in glioma biological functions. Our results will accelerate the understanding of tumorigenesis, cancer progression and even therapeutic targeting in glioblastoma. We hope to inspire researchers to study the role of non-coding RNAs in glioblastoma.
2016-08-30 | GSE86202 | GEO
Project description:To identify the genes significantly regulated by Akt1 activation in NSCLC, myr-Akt1 stable over-expressed A549, HCC827 cells and control vector cells were constructed. The transcriptomes were analyzed by rRNA-depleted strand specific RNA-seq, and LINC01546 was identified significantly up-regulated in myr-Akt1 A549 and HCC827 cells, as compared to vector cells.
2019-11-01 | GSE136904 | GEO
Project description:Background: The receptor tyrosine kinase (RTK) EGFR is overexpressed and mutated in NSCLC. These mutations can be targeted by RTK inhibitors (TKIs) such as erlotinib. Chromatin-modifying agents may offer a novel therapeutic approach by sensitizing tumor cells to TKIs. Methods: The NSCLC cell lines HCC827 (EGFR mutant, adenocarcinoma), A549 (EGFR wt, adenocarcinoma) andNCI-H460 (EGFR wt, large cell carcinoma) were analyzed by SNP6.0 array. Changes in proliferation after panobinostat (LBH-589, PS) and erlotinib treatment were quantified by WST-1 assay and apoptosis by Annexin V/7-AAD flow cytometry. Abundance of target proteins and histone marks (acH3, H3K4me1/2/3) was determined by immunoblotting. Results: As expected, the EGFR wt cell lines A549 and NCI-H460 were quite insensitive to the growth-inhibitory effect of single-agent erlotinib (IC50 70-100 μM), compared to HCC827 (IC50 < 0.02 μM). PS treatment diminished growth to <50 % in both EGFR wt cells, and <30 % in HCC827. The combination of both drugs reduced proliferation by >95 % in HCC827, ≥70 % in A549, but not further in NCI-H460. PS alone induced differentiation and expression of p21WAF1/CIP1 and p53 and decreased CHK1 in all three cell lines, with almost no further effect when combined with erlotinib. In contrast, combination treatment additively decreased pEGFR, pERK, pAKT in A549, and synergistically induced acH3 in both adenocarcinoma lines. Surprisingly, we saw an induction of H3K4 methylation marks after erlotinib treatment in HCC827 (and to a lesser extent in A549) that was even further enhanced by combination with PS. Conclusion: We were able to show that PS synergistically sensitized lung adenocarcinoma cells to the antiproliferative effects of erlotinib. Since single-agent erlotinib has only modest clinical effects in lung adenocarcinoma EGFR wt patients, its combination with an HDACi might offer a promising therapy approach.
2014-12-03 | GSE63784 | GEO