Ectopic Osx+ Cells Affect Tumor Growth
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA600980 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10882500.fastq.gz | Fastqsanger.gz | |||
| SRR10882501.fastq.gz | Fastqsanger.gz | |||
| SRR10882502.fastq.gz | Fastqsanger.gz | |||
| SRR10882503.fastq.gz | Fastqsanger.gz | |||
| SRR10882504.fastq.gz | Fastqsanger.gz |
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Project description:Tumor growth and metastases are dependent on interactions between cancer cells and the local environment. Expression of the cell-cell adhesion molecule N-cadherin (Ncad) is associated with highly aggressive cancers, and its expression by osteogenic cells has been proposed to provide a molecular “dock” for disseminated tumor cells to establish pre-metastatic niches within the bone. Contrary to expectations, the breast cancer cells were able to form tumors in bone and to induce osteolysis in Cdh2-cKO as well as in control mice. Notably, subcutaneous tumors grew larger in Cdh2-cKO relative to control littermates. Cell tracking experiments using the Ai9 reporter revealed the presence of Osx+ and Ncad+ cells in the stroma of extra-skeletal tumors and in a small population of lung cells, a frequent site of breast cancer metastasis. Gene expression analysis by RNAseq of CD45- Osx+ cells isolated from extra-skeletal tumors revealed alterations of pro-tumorigenic signaling pathways in Cdh2-cKO cells relative to control Osx+ cells. Also surprisingly, we find Osx+ cells present in the circulation, and the majority of tumor-associated and circulating Osx+ cells express the hematopoietic marker CD45, have a phenotypic profile resembling that of tumor infiltrating myeloid and lymphoid populations, but with higher expression of lymphocytic immune suppressive genes. Our results indicate that Osx marks distinct tumor promoting CD45- and CD45+ populations and challenge the dogma that osteogenic and hematopoietic markers are mutually exclusive. They also show that Ncad in CD45- Osx+ cells is not necessary for the establishment of bone metastases, but in extra-skeletal tumors it regulates pro-tumorigenic support by the microenvironment.
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Project description:Hippo signaling instructs ectopic but not normal organ growth
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Project description:Cancer cells have abnormal gene expression profiles, however, the transcription factors and the architecture of the regulatory network that drive cancer specific gene expression is often not known. Here we studied a model of Ras-driven invasive tumorigenesis in Drosophila epithelial tissues and combined in vivo genetics with high-throughput sequencing and computational modeling to decipher the regulatory logic of tumor cells. Surprisingly, we discovered that the bulk of the tumor specific gene expression is driven by an ectopic network of a few transcription factors that are overexpressed and/or hyperactivated in tumor cells. These factors are Stat, AP-1, the bHLH proteins Myc and AP-4, the nuclear hormone receptor Ftz-f1, the nuclear receptor coactivator Taiman/AIB1, and Mef2. Notably, many of these transcription factors are also hyperactivated in human tumors. Bioinformatics analysis predicted that these factors directly regulate the majority of the tumor specific gene expression, that they are interconnected by extensive cross-regulation, and that they show a high degree of co-regulation of target genes. Indeed, the factors of this network were required in multiple epithelia for tumor growth and invasiveness and knock-down of individual factors caused a reversion of the tumor specific expression profile, but had no observable effect on normal tissues. We further found that the Hippo pathway effector Yki/Sd was strongly activated in tumor cells and initiated cellular reprogramming by activating several transcription factors of this network. Thus, modeling regulatory networks identified an ectopic yet highly ordered network of master regulators that control tumor cell specific gene expression. RNA-seq gene expression profiling across Drosophila 3rd instar larval imaginal discs in a control and different genetic perturbations.
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Project description:These selections of models are described in the paper:
Cellular interactions constrain tumor growth
by Jeffrey West and Paul K. Newton
Significance:
A mathematical model relating tumor heterogeneity at the cellular level to tumor growth at the macroscopic level is described based on a statistical mechanics framework. The model takes into account the number of accessible states available to each cell as well as their long-range coupling (population cooperation) to other cells. We show that the degree to which cell populations cooperate determines the number of independent cell states, which in turn dictates the macroscopic (volumetric) growth law. It follows that targeting cell-to-cell interactions or functional coupling among cell populations could be a way of mitigating and controlling tumor growth.
Abstract:
A tumor is made up of a heterogeneous collection of cell types, all competing on a fitness landscape mediated by microenvironmental conditions that dictate their interactions. Despite the fact that much is known about cell signaling, cellular cooperation, and the functional constraints that affect cellular behavior, the specifics of how these constraints (and the range over which they act) affect the macroscopic tumor growth laws that govern total volume, mass, and carrying capacity remain poorly understood. We develop a statistical mechanics approach that focuses on the total number of possible states each cell can occupy and show how different assumptions on correlations of these states give rise to the many different macroscopic tumor growth laws used in the literature. Although it is widely understood that molecular and cellular heterogeneity within a tumor is a driver of growth, here we emphasize that focusing on the functional coupling of states at the cellular level is what determines macroscopic growth characteristics.
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2025-01-08 | GSE256016 | GEO
Project description:Cancer cells have abnormal gene expression profiles, however, the transcription factors and the architecture of the regulatory network that drive cancer specific gene expression is often not known. Here we studied a model of Ras-driven invasive tumorigenesis in Drosophila epithelial tissues and combined in vivo genetics with high-throughput sequencing and computational modeling to decipher the regulatory logic of tumor cells. Surprisingly, we discovered that the bulk of the tumor specific gene expression is driven by an ectopic network of a few transcription factors that are overexpressed and/or hyperactivated in tumor cells. These factors are Stat, AP-1, the bHLH proteins Myc and AP-4, the nuclear hormone receptor Ftz-f1, the nuclear receptor coactivator Taiman/AIB1, and Mef2. Notably, many of these transcription factors are also hyperactivated in human tumors. Bioinformatics analysis predicted that these factors directly regulate the majority of the tumor specific gene expression, that they are interconnected by extensive cross-regulation, and that they show a high degree of co-regulation of target genes. Indeed, the factors of this network were required in multiple epithelia for tumor growth and invasiveness and knock-down of individual factors caused a reversion of the tumor specific expression profile, but had no observable effect on normal tissues. We further found that the Hippo pathway effector Yki/Sd was strongly activated in tumor cells and initiated cellular reprogramming by activating several transcription factors of this network. Thus, modeling regulatory networks identified an ectopic yet highly ordered network of master regulators that control tumor cell specific gene expression. RNA-seq gene expression profiling across Drosophila 3rd instar larval wild type wing discs and genetic perturbations of wts.
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Project description:Hippo signaling instructs ectopic but not normal organ growth [Liver YapHyper]
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Project description:Hippo signaling instructs ectopic but not normal organ growth [Drosophila YkiHyper]
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