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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.

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

Project description:Phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway activation contributes to mantle cell lymphoma (MCL) pathogenesis and drug resistance. However, the use of mTOR inhibitors as single agents have shown limited clinical efficacy in relation with drug activation of feedback loops. Selective PI3K inhibition or dual PI3K/mTOR catalytic inhibition are different therapeutic approaches developed to achieve effective pathway blockage. Here, we evaluated the antitumor activity of a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor in primary MCL cells. We found that dual PI3K/mTOR inhibitor modulated angiogenesis, tumor invasiveness and cytokine signaling compared to a mTOR inhibitor and a pan-PI3K inhibitor in MCL. We used microarrays to compare the effect of these three compounds in MCL and identified distinct classes of down-regulated genes modulated by each compound. Global RNA expression in primary cells from two MCL patients treated with a mTOR inhibitor, a pan-PI3K inhibitor and a dual PI3K/mTOR inhibitor for 8 hours

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

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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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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