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Transcriptome Analysis of Gene Expression involving C/EBPβ and Olaparib Resistance

ABSTRACT: Transcriptome Analysis of Gene Expression involving C/EBPβ and Olaparib Resistance

PROVIDER: PRJNA644373 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13490000_1.fastq.gz	Fastqsanger.gz
	SRR13490000_2.fastq.gz	Fastqsanger.gz
	SRR13490001_1.fastq.gz	Fastqsanger.gz
	SRR13490001_2.fastq.gz	Fastqsanger.gz
	SRR13490002_1.fastq.gz	Fastqsanger.gz

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Transcriptome Analysis of Gene Expression involving C/EBPβ and Olaparib Resistance

Project description:Poly(ADP-ribose) polymerase inhibitors (PARPi) are now widely used in treating ovarian cancer. However, PARPi resistance emerges gradually. To investigate the change of gene expression during the transition, we have induced a stable resistant cell strain by culturing A2780 in the continued presence of olaparib. We then performed RNA-seq of the resistant strain and its parent line A2780. We found that C/EBPβ was strongly correlated with PARPi resistance. RNA-seq of C13* after C/EBPβ knockdown was also performed.

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Transcriptome profiling of Olaparib-resistant (OlapR) prostate cancer cell lines

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Project description:PARP inhibitor and platinum based drugs such as cisplatin are promising therapies for triple negative breast cancer and exploit the deficiencies in BRCA1 or BRCA2, or homologous recombination repair defects. However, PARP inhibitor resistance is proven to be a major clinical problem. Acquired PARP inhibitor resistance has been linked with co-resistance to platinum-based drugs. To determine how acquired olaparib resistance affects cisplatin response and whether this is influenced by their BRCA1 status, we performed RNAseq transcriptome analysis of isogenic triple negative breast cancer models of olaparib resistance with normal and mutant BRCA1.

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Olaparib

Project description:Olaparib

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Activation of Wnt signaling promotes olaparib resistant ovarian cancer.

Project description:Sequencing of olaparib-resistant PEO1 derivatives (C4, C5, C10 and C18) and parental PEO1 (P1 and P2) cells was performed in order to determine mechanisms of acquired resistance in the resistant cell lines. PEO1 parental cell lines were authenticated prior to sequencing. PEO1 parental were confirmed to be BRCA2-mutated (5139C>G). Olaparib PEO1 resistant cells were generated through a step-wise escalation of olaparib (10nM to 8uM olaparib). In olaparib resistant lines an increase canonical Wnt signaling and loss of of non-canonical Wnt signaling was observed.

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Project description:Analysis of enzalutamide- and/or olaparib-responsive gene expression in prostate cancer cells. The hypothesis tested in the present study was that enzalutamide influences the expression of genes that are involved in important bioprocesses in prostate cance rcells, including DNA damage response genes and this effect may synergize with poly(ADP-ribose) polymerase inhibitor olaparib in cytotoxicity to prstate cancer cells. prostate cancer cells were pretreated with enzalutamide or vehicle control DMSO for 24 h, followed by treatment with enzalutamide, olaparib, enzalutamide+olaparib, or vehicle control DMSO for 48 h. Gene expression in enzalutamide+olaparib-treated cells was compared with taht in vehicle control- and single agent-treated cells.

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Project description:Olaparib resistance and cisplatin responses in triple negative breast cancer

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Deregulation of the endogenous C/EBPβ LIP isoform predisposes to tumorigenesis

Project description:Two long and one truncated isoforms (termed LAP*, LAP, and LIP, respectively) of the transcription factor CCAAT enhancer binding protein beta (C/EBPβ) are expressed from a single intronless Cebpb gene by alternative translation initiation. Isoform expression is sensitive to mammalian target of rapamycin (mTOR)-mediated activation of the translation initiation machinery and relayed through an upstream open reading frame (uORF) on the C/EBPβ mRNA. The truncated C/EBPβ LIP, initiated by high mTOR activity, has been implied in neoplasia, but it was never shown whether endogenous C/EBPβ LIP may function as an oncogene. In this study, we examined spontaneous tumor formation in C/EBPβ knockin mice that constitutively express only the C/EBPβ LIP isoform from its own locus. Our data show that deregulated C/EBPβ LIP predisposes to oncogenesis in many tissues. Gene expression profiling suggests that C/EBPβ LIP supports a protumorigenic microenvironment, resistance to apoptosis, and alteration of cytokine/chemokine expression. The results imply that enhanced translation reinitiation of C/ EBPβ LIP promotes tumorigenesis. Accordingly, pharmacological restriction of mTOR function might be a therapeutic option in tumorigenesis that involves enhanced expression of the truncated C/EBPβ LIP isoform.

2014-12-16 | GSE53770 | GEO

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