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YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells.

ABSTRACT: YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells.

PROVIDER: PRJNA940048 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23652864.fastq.gz	Fastqsanger.gz
	SRR23652865.fastq.gz	Fastqsanger.gz
	SRR23652866.fastq.gz	Fastqsanger.gz
	SRR23652867.fastq.gz	Fastqsanger.gz
	SRR23652868.fastq.gz	Fastqsanger.gz

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YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RPPA]

Project description:In heterogeneous head and neck cancer (HNC), subtype-specific treatment regimens are currently missing. An integrated analysis of patient HNC subtypes using single-cell sequencing and proteome profiles revealed an epithelial-mesenchymal transition (EMT) signature within the epithelial cancer-cell population. The EMT signature coincided with PI3K/mTOR inactivation in the mesenchymal subtype. Conversely, the signature was suppressed in epithelial cells of the basal subtype which exhibits hyperactive PI3K/mTOR signalling. We further identified YBX1 phosphorylation, downstream of the PI3K/mTOR pathway, restrains basal-like cancer cell proliferation. In contrast, YBX1 acts as a safeguard against the proliferation-to-invasion switch in mesenchymal-like epithelial cancer cells, and its loss accentuates partial-EMT and in vivo invasion. Interestingly, phospho-YBX1 that is mutually exclusive to partial-EMT, emerged as a prognostic marker for overall patient outcomes. Expression profiling by reverse-phase protein array were performed to explore the underlying molecular mechanisms.

2023-03-03 | GSE226356 | GEO

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RNA-seq]

Project description:In heterogeneous head and neck cancer (HNC), subtype-specific treatment regimens are currently missing. An integrated analysis of patient HNC subtypes using single-cell sequencing and proteome profiles revealed an epithelial-mesenchymal transition (EMT) signature within the epithelial cancer-cell population. The EMT signature coincided with PI3K/mTOR inactivation in the mesenchymal subtype. Conversely, the signature was suppressed in epithelial cells of the basal subtype which exhibits hyperactive PI3K/mTOR signalling. We further identified YBX1 phosphorylation, downstream of the PI3K/mTOR pathway, restrains basal-like cancer cell proliferation. In contrast, YBX1 acts as a safeguard against the proliferation-to-invasion switch in mesenchymal-like epithelial cancer cells, and its loss accentuates partial-EMT and in vivo invasion. Interestingly, phospho-YBX1 that is mutually exclusive to partial-EMT, emerged as a prognostic marker for overall patient outcomes. Expression profiling by high throughputsequencing were performed to explore the underlying molecular mechanisms.

2023-03-03 | GSE226355 | GEO

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RPPA]

Project description:YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RPPA]

| PRJNA940055 | ENA

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RNA-seq]

Project description:YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells [RNA-seq]

| PRJNA940054 | ENA

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells.

Project description:In heterogeneous head and neck cancer (HNC), subtype-specific treatment regimens are currently missing. An integrated analysis of patient HNC subtypes using single-cell sequencing and proteome profiles reveals an epithelial-mesenchymal transition (EMT) signature within the epithelial cancer-cell population. The EMT signature coincides with PI3K/mTOR inactivation in the mesenchymal subtype. Conversely, the signature is suppressed in epithelial cells of the basal subtype which exhibits hyperactive PI3K/mTOR signalling. We further identify YBX1 phosphorylation, downstream of the PI3K/mTOR pathway, restraining basal-like cancer cell proliferation. In contrast, YBX1 acts as a safeguard against the proliferation-to-invasion switch in mesenchymal-like epithelial cancer cells, and its loss accentuates partial-EMT and in vivo invasion. Interestingly, phospho-YBX1 that is mutually exclusive to partial-EMT, emerges as a prognostic marker for overall patient outcomes. These findings create a unique opportunity to sensitise mesenchymal cancer cells to PI3K/mTOR inhibitors by shifting them towards a basal-like subtype as a promising therapeutic approach against HNC.

| S-EPMC10033729 | biostudies-literature

YBX1 integration of oncogenic PI3K/mTOR signalling regulates the fitness of malignant epithelial cells.

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

2023-03-03 | GSE226357 | GEO

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

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2013-12-14 | E-GEOD-53309 | biostudies-arrayexpress

Comparative study of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in MCL

2013-12-14 | GSE53309 | GEO

Omipalisib Inhibits Esophageal Cancer Growth through PI3K/AKT/mTOR Signalling Pathway Disruption

Project description:Esophageal squamous cell carcinoma (OSCC) is a lethal digestive tract malignancy with limited effective interventions. This study aims to explore a new potential inhibitor on OSCC and investigate the underlying mechanisms. Based on a drug screen of an FDA-proven library consisting of 1404 compounds, we demonstrated that Omipalisib, a dual PI3K/mTOR inhibitor, markedly inhibited cell proliferation and colony formation in a panel of OSCC cell lines. Mechanistically, Omipalisib induced G0/G1 phase cell cycle arrest and apoptosis. Moreover, RNA-seq, KEGG and GSEA confirmed that the PI3K/mTOR signalling pathway is the primary target of Omipalisib in OSCC cells. Omipalisib treatment suppressed the PI3K/mTOR signalling pathway. Furthermore, Omipalisib exerted a significant antineoplastic effect on OSCC tumour xenografts in BALB/c nude mice without obvious side effects. The present study supports the rationale for using Omipalisib as a therapeutic approach for OSCC cases and suggests the potential clinical evaluation of this strategy.

2020-01-11 | GSE143462 | GEO

SUM52PE treated with PI3K-mTOR inhibitors

Project description:SUM52PE treated with PI3K-mTOR inhibitors

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