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

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

PROVIDER: PRJNA1041414 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26856544_1.fastq.gz	Fastqsanger.gz
	SRR26856544_2.fastq.gz	Fastqsanger.gz
	SRR26856545_1.fastq.gz	Fastqsanger.gz
	SRR26856545_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

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

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 (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

Bid Expression Controls Neuronal Cell Fate During Avian Ciliary Ganglion Development

Project description:To elucidate molecular networks regulating important aspects of parasympathetic neuronal development, a genome-wide expression analysis was performed during multiple stages of avian ciliary ganglion (CG) development. The transcriptome data showed a well-defined sequence of events, starting from neuronal migration via neuronal fate cell determination, synaptic transmission, regulation of synaptic plasticity to growth factor associated signaling. Focusing on cell death-related changes in the transcriptome, we could characterize a series of events that starts with the activation of neuronal apoptotic processes at E7 via the cell death execution phase at E8 and E9 and ends with apoptotic cell clearance at E14. Moreover, we detected a transient up-regulation of the transcription factors TP53 and RARB that was linked to cell death. The expression of BID, a p53 target, was also found to be dynamically regulated. Using a virus-based RNAi knockdown approach, BID expression was shown to be crucial for the execution of ontogenetic programmed cell death (PCD). Therefore, this study for the first time provides a comprehensive analysis of CG neuron development on the transcriptome level, revealing a temporally well-controlled expression of genes regulating ontogenetic PCD, with BID being one of the most dynamically regulated genes during the cell death phase. The effect of BID silencing in vivo suggests an essential role of BID expression in neuronal development.

2018-06-20 | GSE65426 | GEO

BID is critical for IFN-alpha-induced cell death

Project description:Clinical applications of human interferon (IFN)-alpha have met with varying degrees of success. Nevertheless, key molecules in IFN-alpha-induced cell death have not been clearly identified. Our previous study indicated that IFN (alpha, beta and omega) receptor (IFNAR) 1/2- and IFN regulatory factor (IRF) 9-RNA interference (RNAi) completely inhibited the antiproliferative (AP) activity of IFN-alpha in human ovarian adenocarcinoma OVCAR3 cells sensitive to IFN-alpha., followed by transcription of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Here, IFNAR1/2- and IRF9-RNAi inhibited the gene expression of TRAIL, but not of Fas ligand (FasL), following IFN-alpha treatment. In fact, TRAIL but not FasL inhibited the proliferation of OVCAR3 cells. IFN-alpha notably up-regulated the levels of TRAIL protein in the supernatant and on the membrane of OVCAR3 cells. Following TRAIL signaling, Caspase 8 inhibitor and BH3 interacting domain death agonist (BID)-RNAi significantly abrogated both AP activities of IFN-alpha and TRAIL. Furthermore, BID-RNAi prevented both IFN-alpha and TRAIL from collapsing the mitochondrial membrane potential (Delta Psi m). Finally, we provide important new evidence that BID overexpression led to a major enhancement of both AP activities of IFN-alpha and TRAIL in human lung carcinoma A549 cells resistant to IFN-alpha. Thus, this study suggests that BID is crucial in IFN-alpha-induced cell death, indicating a notable potential to be a targeted therapy for IFN-alpha resistant tumors.

2012-05-22 | GSE29790 | GEO

Analysis of the inflammatory transcription profiles of WT and Bid microglia

Project description:Apoptosis is a controlled cell-death process mediated inter alia by proteins of the Bcl-2 family. Some proteins previously shown to promote the apoptotic process were found to have non-apoptotic functions as well. Microglia, the resident immune cells of the central nervous system, respond to brain derangements by becoming activated to contend with the brain damage. Activated microglia can also undergo activation-induced cell death. Previous studies have addressed the role of core apoptotic proteins in the death process, but whether or not these proteins also play a role in the activation process has not been reported. Here we explore the effect of the BH3-only protein Bid on the immunological features of microglia by subjecting both WT and Bid deficient primary neonatal microglial cultures to LPS treatment (100 ng/ml, 3h) or left untreated (control) and analyzing their transcription profiles in order to study the role of Bid. 4 samples were analyzed. no replication.

2010-09-01 | E-GEOD-18108 | biostudies-arrayexpress

BID-seq for transcriptome-wide quantitative sequencing of mRNA pseudouridine at base resolution

Project description:Pseudouridine (Ψ) is an abundant RNA modification that is present in and impacts the functions of diverse non-coding RNA species, including rRNA, tRNA, snRNA, etc. Pseudouridine also exists in mammalian mRNA and likely exhibits functional roles; however, functional investigations of pseudouridine in mammalian mRNA have been hampered by the lack of a quantitative method that detects Ψ at base precision. We have recently developed Bisulfite-Induced Deletion sequencing (BID-seq), which provides the community with a quantitative method to map RNA Ψ distribution transcriptome-wide at single-base resolution. Here, we describe an optimized BID-seq protocol to generate highly reproducible results, displaying nearly zero background deletions at unmodified uridines after bisulfite treatment and uncovering 8,407 Ψ sites starting from as little as 10 ng mouse embryonic stem cell (mESC) polyA+ RNA, with the steps that are fast in both library preparation and data analysis. This optimized BID-seq workflow takes 5 days to complete and includes four main sections: RNA preparation, library construction, next-generation sequencing (NGS), and data analysis. The library construction can be completed by researchers who have basic knowledge and skills in molecular biology and genetics. In addition to the experimental protocol, we provide BID-pipe (https://github.com/y9c/pseudoU-BIDseq), a user-friendly data analysis pipeline for BID-seq, requiring only basic bioinformatic and computational skills to uncover Ψ signatures from NGS data.

2023-08-07 | GSE238245 | GEO

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