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Knockdown of the long noncoding RNA PURPL induces apoptosis and sensitizes liver cancer cells to doxorubicin

ABSTRACT: Knockdown of the long noncoding RNA PURPL induces apoptosis and sensitizes liver cancer cells to doxorubicin

PROVIDER: PRJNA770529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16296562_1.fastq.gz	Fastqsanger.gz
	SRR16296562_2.fastq.gz	Fastqsanger.gz
	SRR16296563_1.fastq.gz	Fastqsanger.gz
	SRR16296563_2.fastq.gz	Fastqsanger.gz
	SRR16296564_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Knockdown of the long noncoding RNA PURPL induces apoptosis and sensitizes liver cancer cells to doxorubicin.

Project description:Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer with increasing incidence in western countries. Most HCC patients have advanced cancer at the time of diagnosis due to the asymptomatic nature of early-stage HCC and do not qualify for potentially curative surgical treatment, thus, highlighting the need for new therapeutic strategies. Long noncoding RNAs (lncRNAs) comprise a large and heterogeneous group of non-protein coding transcripts that play important regulatory roles in numerous biological processes in cancer. In this study, we performed RNA sequencing of liver biopsies from ten HCC, ten hepatitis C virus-associated HCC, and four normal livers to identify dysregulated lncRNAs in HCC. We show that the lncRNA p53-upregulated-regulator-of-p53-levels (PURPL) is upregulated in HCC biopsies and that its expression is p53-dependent in liver cancer cell lines. In addition, antisense oligonucleotide-mediated knockdown of PURPL inhibited cell proliferation, induced apoptosis, and sensitized HepG2 human HCC cells to treatment with the chemotherapeutic agent doxorubicin. In summary, our findings suggest that PURPL could serve as a new therapeutic target for reversing doxorubicin resistance in HCC.

| S-EPMC9663437 | biostudies-literature

PURPL Represses Radiation-induced Apoptosis to Promote Radioresistance in Cutaneous Melanoma by Direct Interfering with BID Cleavage

Project description:During the treatment of cutaneous melanoma, the presence of radioresistance compromised the therapeutic effects of radiotherapy. Yet, the mechanism of radioresistance in melanoma still remains unclear. Bioinformatic analysis of the transcriptomic sequencing showed PURPL was top up-regulated genes in response to ionizing radiation (IR) treatment in melanoma cells. Loss of PURPL notably repressed melanoma cell viability, colony formation, migration and invasiveness which potentiated PURPL’s role in radioresistance of melanoma. Further, loss-of- and gain-of-function analysis indicated that PURPL repressed IR-induced DNA damage and apoptosis. Mechanistically, RNA pulldown was performed and BID was identified as the interacting protein partner of PURPL. As the core gene of the mitochondrial apoptosis pathway, BID could be cleaved by Caspase-8 to generate tBID, which promotes the permeability of the mitochondrial membrane and the release of cytochrome c. IR treatment promotes the interaction between BID and Caspase-8 which was further strengthened by the loss of PURPL. The in vivo assays further verified the in vitro findings. Collectively, our study supports the pro-radioresistance role of PURPL in melanoma by inhibiting the interaction between BID and Caspase-8, which may provide a novel target for clinical radiotherapy.

2024-01-01 | GSE248024 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (Iso-Seq)

Project description:The goal of our study is to investigate the role of the p53-induced lncRNA PURPL in the context of liver cancer. To achieve this, we identified transcript variants of PURPL expressed in liver cancer cells and assayed for the transcriptome changes caused by PURPL knockdown after p53 induction.

2022-10-18 | GSE206701 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq II)

2022-10-18 | GSE206699 | GEO

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation (RNA-Seq I)

2022-10-18 | GSE206698 | GEO

Knockdown of the long noncoding RNA PURPL induces apoptosis and sensitizes liver cancer cells to doxorubicin

Project description:Liver cancer was the fourth leading cause of cancer-related deaths worldwide in 2018, of which Hepatocellular carcinoma accounts for 75-85% of all liver cancers and is therefore the most common type of liver cancer. In this study, total RNA were extracted from sections of formalin-fixed paraffin embedded (FFPE) archival human liver biopsies from 24 patients, including ten HCV-associated HCC (HCV-HCC), ten virus-unrelated HCC (VU-HCC) and four normal liver patients. By comparing the expression profiles of HCV-HCC and VU-HCC to that of the normal liver biopsies respectively, 18 lncRNAs were identified to be differentially expressed.

2022-11-21 | GSE185700 | GEO

Identification of PURPL regulated genes in HCT116 cells

Project description:Analysis of changes in gene expression profile upon depletion of PURPL in HCT116 cells. The hypothesis in this study is that PURPL regulates gene expression in the p53 pathway.

2017-08-03 | GSE79053 | GEO

Mass spectrometry (MS) datasets of PURPL RNA pulldown samples in A375 cells

Project description:We performed PURPL RNA pulldown followed by MS analysis to identify purpl-interacting proteins in A375 cells.With high performance liquid chromatography-mass spectrometry (HPLC-MS), the binding protein of PURPL from RNA pull down was detected by removing non-specific protein which were binding with EGFP.

2022-02-16 | PXD028863 | Pride

Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation

Project description:Context-dependent function of long noncoding RNA PURPL in transcriptome regulation during p53 activation

| PRJNA851788 | ENA

Inhibition of dihydroorotate dehydrogenase by doxorubicin and brequinar sensitize cancer cells to TRAIL-induced apoptosis

Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising agent in selectively killing tumor cells. However, TRAIL monotherapy is not especially successful due to the fact that many cancer cells are resistant to TRAIL. Chemotherapeutic agents, such as doxorubicin have been shown to act synergistically with TRAIL on cancer cells, but the exact mechanisms of actions are poorly understood. In this study we performed high-throughput siRNA screening and genome-wide gene expression profiling on doxorubicin treated U1690 cells to explore novel mechanisms underlying doxorubicin-TRAIL synergy. The screening and expression profiling results were integrated and dihydroorotate dehydrogenase (DHODH) was identified to be a potential candidate. DHODH is rate-limiting enzyme in the pyrimidine synthesis pathway, and its expression was downregulated by doxorubicin and silencing of DHODH sensitized U1690 cells to TRAIL. Inhibition of DHODH activity by brequinar dramatically increased the sensitivity of U1690 cells to TRAIL-induced apoptosis, and was accompanied by downregulation of cFLIPL and mitochondrial depolarization. However, the expressions of DR4 and 5 were not changed in response to brequinar treatment in contrast to doxorubicin. In addition, uridine, an end product of the pyrimidine synthesis pathway was able to rescue the sensitization effects initialized by both brequinar and doxorubicin. Furthermore, other cancer cell lines, LNCaP, MCF-7 and HT-29 were also shown to be sensitized to TRAIL by brequinar. Taken together, our findings have identified a novel drug, brequinar, to be potentially utilized in TRAIL combinatorial cancer therapy and highlighted for the first time the importance of DHODH and pyrimidine pathway in mediating TRAIL sensitization in cancer cells. Total RNA obtained from small cell lung cancer U1690 cells either treated with DMSO control or 1 M-BM-5M doxorubicin for 12 or 24h.

2013-06-01 | E-GEOD-42531 | biostudies-arrayexpress

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