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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (RNA-seq)

ABSTRACT: Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (RNA-seq)

PROVIDER: PRJNA484869 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7651700_1.fastq.gz	Fastqsanger.gz
	SRR7651700_2.fastq.gz	Fastqsanger.gz
	SRR7651710_1.fastq.gz	Fastqsanger.gz
	SRR7651710_2.fastq.gz	Fastqsanger.gz
	SRR7651720_1.fastq.gz	Fastqsanger.gz

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PARCB Project: Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage.

Project description:The use of potent therapies inhibiting critical oncogenic pathways active in epithelial cancers has led to multiple resistance mechanisms, including the development of highly aggressive, small cell neuroendocrine carcinoma (SCNC). SCNC patients have a dismal prognosis due in part to a limited understanding of the molecular mechanisms driving this malignancy and the lack of effective treatments. Here, we demonstrate that a common set of defined oncogenic drivers reproducibly reprograms normal human prostate and lung epithelial cells to small cell prostate cancer (SCPC) and small cell lung cancer (SCLC), respectively. We identify shared active transcription factor binding regions in the reprogrammed prostate and lung SCNCs by integrative analyses of epigenetic and transcriptional landscapes. These results suggest that neuroendocrine cancers arising from distinct epithelial tissues may share common vulnerabilities that could be exploited for the development of drugs targeting SCNCs.

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (RNA-seq)

Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage (ATAC-seq)

Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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Project description:Small cell carcinomas from different tissues exhibit transcriptional and epigenetic convergence and suggest common vulnerabilities for therapies

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PARCB Project: Reprogramming normal human epithelial tissues to a common, lethal neuroendocrine cancer lineage

Project description:This SuperSeries is composed of the SubSeries listed below.

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Proteome-wide profiling study unmasked lineage-based and clinical feature-based molecular landscapes of pituitary neuroendocrine tumors

Project description:Pituitary neuroendocrine tumors (PitNETs) account for the second most common intracranial tumors. Currently, there is still a lack of comprehensive understanding regarding the molecular mechanisms associated with lineage or clinical features of PitNETs, which hinders development of effective treatment strategies. Herein, we performed in-depth proteome profiling of 68 PitNET tumors and 4 pituitary glands. We systematically investigated the common and specific aberrant biological mechanisms in TPIT (ACTH/SCA) and PIT1 (TSH/PRL/GH) lineages. Our findings revealed that Wnt signaling pathway and MAPK signaling pathway played crucial regulatory roles in both lineages, while lipid metabolism abnormalities were more prominent in TPIT lineage, and decreased cell adhesion was more significant in PIT1 lineage. Based on these findings, we delved into the interactions between drugs and proteins to explore reliable drug targets and treatment options. We identified 17 potential drug targets and 51 FDA-approved drugs in TPIT lineage, and 19 potential drug targets and 97 FDA-approved drugs in PIT1 lineage, respectively. Additionally, we reclassified the samples based on 4 important clinical phenotypes: invasiveness, recurrence, high incidence in women of childbearing age, and tumor stiffness. By combining artificial intelligence (AI) and bioinformatics analysis, we further investigated the related mechanistic information. Our results highlighted the close association of abnormal neuronal activity with tumor invasiveness, as well as the intimate correlation between cell adhesion alterations and the other 3 clinical phenotypes. Overall, our study provides valuable insights into both of lineage-based and clinical feature-based pathophysiological mechanisms of PitNETs, and offers novel reference for future targeted therapies.

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