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

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

PROVIDER: PRJNA672677 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12914520.fastq.gz	Fastqsanger.gz
	SRR12914521.fastq.gz	Fastqsanger.gz
	SRR12914522.fastq.gz	Fastqsanger.gz
	SRR12914523.fastq.gz	Fastqsanger.gz
	SRR12914524.fastq.gz	Fastqsanger.gz

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

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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

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

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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.

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