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

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

PROVIDER: PRJNA940055 | ENA |

REPOSITORIES: ENA

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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.

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

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

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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]

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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

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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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SUM52PE treated with PI3K-mTOR inhibitors

Project description:SUM52PE treated with PI3K-mTOR inhibitors

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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