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Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

ABSTRACT: Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

PROVIDER: PRJNA796277 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17549866.fastq.gz	Fastqsanger.gz
	SRR17549867.fastq.gz	Fastqsanger.gz
	SRR17549868.fastq.gz	Fastqsanger.gz
	SRR17549869.fastq.gz	Fastqsanger.gz
	SRR17549870.fastq.gz	Fastqsanger.gz

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Similar Datasets

Death Receptor 5 Antisense Long Noncoding RNA and Cisplatin Modulate Macromolecular and Metabolic Changes in HeLa Cells

Project description:We have performed a transcriptomics study in which we first apply cisplatin to HeLa cells. Total RNA was isolated from control as well as treated cells and apoptosis was confirmed by Annexin V and 7AAD staining in flow cytometry. Total RNAs were subjected to deep-sequencing to identify differentially expressed mRNAs. We then took advantage of bioinformatic tools to identify which pathways are affected by Cisplatin treatment

2024-01-17 | GSE193447 | GEO

Knockdown of death receptor 5 antisense long noncoding RNA and cisplatin treatment modulate similar macromolecular and metabolic changes in HeLa cells.

Project description:Background/aimDespite great progress in complex gene regulatory mechanisms in the dynamic tumor microenvironment, the potential contribution of long noncoding RNAs (lncRNAs) to cancer cell metabolism is poorly understood. Death receptor 5 antisense (DR5-AS) is a cisplatin inducible lncRNA whose knockdown modulates cell morphology. However, its effect on cell metabolism is unknown. The aim of this study is to examine metabolic changes modulated by cisplatin and DR5-AS lncRNA in HeLa cells.Materials and methodsWe used cisplatin as a universal cancer therapeutic drug to modulate metabolic changes in HeLa cervix cancer cells. We then examined the extent of metabolic changes by Fourier transform infrared spectroscopy (FTIR). We also performed transcriptomics analyses by generating new RNA-seq data with total RNAs isolated from cisplatin-treated HeLa cells. Then, we compared cisplatin-mediated transcriptomics and macromolecular changes with those mediated by DR5-AS knockdown.ResultsCisplatin treatment caused changes in the unsaturated fatty acid and lipid-to-protein ratios and the glycogen content. These observations in altered cellular metabolism were supported by transcriptomics analyses. FTIR spectroscopy analyses have revealed that DR5-AS knockdown causes a 20.9% elevation in the lipid/protein ratio and a 76.6% decrease in lipid peroxidation. Furthermore, we detected a 3.42% increase in the chain length of the aliphatic lipids, a higher content of RNA, and a lower amount of glycogen indicating relatively lower metabolic activity in the DR5-AS knockdown HeLa cells. Interestingly, we observed a similar gene expression pattern under cisplatin treatment and DR5-AS knockdown HeLa cells.ConclusionThese results suggest that DR5-AS lncRNA appears to account for a fraction of cisplatin-mediated macromolecular and metabolic changes in HeLa cervix cancer cells.

| S-EPMC10387844 | biostudies-literature

Cisplatin-inducible death receptor 5 antisense long non-coding RNA modulates cell cycle and proliferation in HeLa cells

Project description:Cisplatin-inducible death receptor 5 antisense long non-coding RNA modulates cell cycle and proliferation in HeLa cells

| PRJNA672677 | ENA

Gene Expression in Cisplatin Resistance HeLa Cells

Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.

2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress

Gene Expression in Cisplatin Resistance HeLa Cells

2010-03-05 | GSE15120 | GEO

Gene expression data from parental HeLa and Dickkopf-1 (Dkk1) knockout HeLa cells after Cisplatin treatment

Project description:Infection with oncogenic human papillomavirus (HPV) is a major cause for the development of cervical cancer, which is mainly driven by the expression of the HPV E6 and E7 oncoproteins. We uncovered that the concentration levels of the putative tumor suppressor Dickkopf-1 (Dkk1) are restricted in cervical cancer cells by HPV E6 expression due to the E6-mediated proteolytic degradation of p53, which is a transcriptional regulator of Dkk1. Moreover, we found that Dkk1 is critically involved in the pro-apoptotic Cisplatin response of these cells, as Dkk1 repression was associated with an increased resistance towards the chemotherapeutic compound. This could be of high relevance for cervical cancer treatments, which usually involve Cisplatin for standard care. Although Dkk1 is a major antagonist of the canonical Wnt signaling, the differential response towards Cisplatin observed in Dkk1-depleted cells was not associated to an activation of this pathway. To elucidate alternative underlying mechanisms, we performed Affymetrix Gene Expression analyses comparing the transcriptome of Cisplatin-treated parental HeLa to CRISPR/Cas9-generated Dkk1 knockout (KO) HeLa cells. These revealed that Dkk1 depletion is linked to an impairment of the pro-apoptotic JNK/AP-1 pathway in cervical cancer cells, suggesting that Dkk1 drives Cisplatin-mediated apoptosis via activation of this signaling hub.

2022-08-16 | GSE200748 | GEO

Transcriptomics Profiling Identifies Cisplatin-Inducible Death Receptor 5 Antisense Long Non-coding RNA as a Modulator of Proliferation and Metastasis in HeLa Cells.

Project description:Cisplatin is a well-known cancer chemotherapeutic agent but how extensively long non-coding RNA (lncRNA) expression is modulated by cisplatin is unknown. It is imperative to employ a comprehensive approach to obtain a better account of cisplatin-mediated changes in the expression of lncRNAs. In this study, we used a transcriptomics approach to profile lncRNAs in cisplatin-treated HeLa cells, which resulted in identification of 10,214 differentially expressed lncRNAs, of which 2,500 were antisense lncRNAs. For functional analyses, we knocked down one of the cisplatin inducible lncRNAs, death receptor 5 antisense (DR5-AS) lncRNA, which resulted in a morphological change in HeLa cell shape without inducing any cell death. A second round of transcriptomics-based profiling revealed differential expression of genes associated with immune system, motility and cell cycle in DR5-AS knockdown HeLa cells. Cellular analyses showed that DR5-AS reduced cell proliferation and caused a cell cycle arrest at S and G2/M phases. Moreover, DR5-AS knockdown reduced the invasive capacity of HeLa cells in zebrafish xenograft model. These results suggest that cisplatin-mediated pleiotropic effects, such as reduction in cell proliferation, metastasis and cell cycle arrest, may be mediated by lncRNAs.

| S-EPMC8419520 | biostudies-literature

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (miRNA)

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.

2013-01-15 | E-GEOD-43249 | biostudies-arrayexpress

Noncoding RNA expression profiling of cisplatin-resistant cells derived from the A549 lung cell line (lncRNA and mRNA)

2013-01-15 | E-GEOD-43493 | biostudies-arrayexpress

Cisplatin-inducible death receptor 5 antisense long non-coding RNA modulates cell cycle and proliferation in HeLa cells

Project description:We have performed a transcriptomics study in which we first transfected LNA GapmeRs against DR5-AS lncRNA to silence it in HeLa cells. Total RNA was isolated from control as well as transfected cells and silencing was confirmed by qPCR. Total RNAs were subjected to deep-sequencing to identify differentially expressed mRNAs. We then took advantage of bioinformatic tools to identify which pathways are affected by DR5-AS knock-down.

2021-04-01 | GSE160227 | GEO

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