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Network Biology of Tumor Stem-like Cells Identified a Regulatory Role of CBX5 in Lung Cancer

ABSTRACT: Mounting evidence points to a link between a cancer possessing stem-like properties and a worse prognosis. To understand the biology, a common approach is to integrate network biology with signal processing mechanics. That said, even with the right tools, predicting the risk for a highly susceptible target using only a handful of gene signatures remains very difficult. By compiling the expression profiles of a panel of tumor stem-like cells (TSLCs) originating in different tissues, comparing these to their parental tumor cells (PTCs) and the human embryonic stem cells (hESCs), and integrating network analysis with signaling mechanics, we propose that network topologically-weighted signaling processing measurements under tissue-specific conditions can provide scalable and predicable target identification. All function codes related to this project could be accessed at the supplementary website.

ORGANISM(S): Homo sapiens

PROVIDER: GSE35603 | GEO | 2012/08/17

SECONDARY ACCESSION(S): PRJNA152527

REPOSITORIES: GEO

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Network Biology of Tumor Stem-like Cells Identified a Regulatory Role of CBX5 in Lung Cancer

Project description:Mounting evidence points to a link between a cancer possessing stem-like properties and a worse prognosis. To understand the biology, a common approach is to integrate network biology with signal processing mechanics. That said, even with the right tools, predicting the risk for a highly susceptible target using only a handful of gene signatures remains very difficult. By compiling the expression profiles of a panel of tumor stem-like cells (TSLCs) originating in different tissues, comparing these to their parental tumor cells (PTCs) and the human embryonic stem cells (hESCs), and integrating network analysis with signaling mechanics, we propose that network topologically-weighted signaling processing measurements under tissue-specific conditions can provide scalable and predicable target identification. All function codes related to this project could be accessed at the supplementary website. We hypothesized that the transcriptional stochastic element of lung tumors modeled by the lung-TSLC networks could be utilized to estimate the prognostic survival times. A scalable, network-based signal-processing model was devised to analyze the transcriptional signal for a single gene or for a set of genes relating to other gene players in the networks. We tested our hypothesis in the following three steps: (1) construct the consensus TSLC networks and the lung-TSLC networks by analyzing the transcriptomes of three panels of cells: the parental tumor cells (PTCs), the cultivated TSLCs, and the human embryonic stem cels (hESCs); (2) develop network topologically-weighted signal processing measurements and apply such measurements to find the survival correlation and to identify potential targets for biological validation; and (3) verify a potential regulatory target - Cbx5 - in another clinical cohort of LACs as well as in knock-down experiments in lung TSLCs functional assays and in animal models.

2012-08-17 | E-GEOD-35603 | biostudies-arrayexpress

Folsomia candida soil analysis expression assay

Project description:The present invention relates to methods for determining soil quality, and especially soil pollution, using the invertebrate soil organism Folsomia candida also designated as springtail. Specifically, the present invention relates to a method for determining soil quality comprising: contacting Folsomia Candida with a soil sample to be analysed during a time period of 1 to 5 days; isolating said soil contacted Folsomia Candida; extracting RNA from said isolated soil contacted Folsomia Candida; determing a gene expression profile based on said extracted RNA using microarray technology; comparing said gene expression profile with a reference gene expression profile; and determing soil quality based expression level differences between said gene expression profile and said control expression profile.

2014-07-19 | GSE59588 | GEO

Plexin-B2 regulates mechanotension during multicellular organization

Project description:During multicellular organization, individual cells need to constantly adjust intracellular contractility and junctional adhesive properties in order to maintain tissue cohesion and mechanotension. The membrane receptors linking external biochemical cues and internal cell mechanics are incompletely understood. Here, we reveal that the axon guidance receptor Plexin-B2 regulates intracellular mechanotension, and this in turn impacts cell-cell/cell-matrix adhesiveness during self-assembly of human embryonic stem cells (hESCs) and neuroprogenitor cells (hNPCs) into epithelial structures. The altered tissue mechanics caused by Plexin-B2 deficiency or over expression affects stem cell behaviors as well as β-catenin and YAP mechanosensing. Strikingly, Plexin-B2 deficiency results in accelerated neuronal differentiation, while proper levels of Plexin-B2 activity are required for maintaining cytoarchitectural integrity of the neuroepithelium as modeled in cerebral organoids. Mechanistically, Plexin-B2 engages its extracellular and Ras-GAP domains for mechanoregulation via RAP1/2. Our studies establish mechanoregulation as a key function of Plexin-B2 during multicellular organization, thereby solidifying the principle of force- mediated regulation of stem cell biology and tissue morphogenesis.

2021-09-07 | GSE158017 | GEO

Differentially expression profiling in a brain metastasis of a papillary thyroid carcinoma and its technical replicate vs. non-brain metastatic papillary thyroid carcinomas, and primary brain tumors

Project description:Experiment: Establishment of expression profiles in a brain metastasis from a PTC (RNA processing and hybridization to Affymetrix microarray done twice to yield a technical replicate), in non-brain metastatic, stage III and IV PTCs, and primary brain tumors. Biostatistics analysis identified genes and biofunctions related to the brain metastatic PTC.

2016-11-01 | GSE66463 | GEO

Mus musculus

Project description:Network Biology of the Skin [1]

| PRJNA229159 | ENA

Mus musculus

Project description:Network Biology of the Skin [2]

| PRJNA229538 | ENA

Genome-wide copy number alteration analysis to identify genetic signature for development of distant metastases in Papillary Thyroid Cancer

Project description:With the intent of identify alterations associated with the development of distant metastases in Papillary Thyroid Cancer (PTCs), we design a case-control study and performed genome-wide copy number variation analysis by Affymetrix Oncoscan FFPE Kit on 34 PTCs that developed distant metastases (DM-PTCs), 61 PTCs without distant metastases (CTRL-PTCs), and on 7 tissue from distant metastatic site

2018-03-01 | E-MTAB-5194 | biostudies-arrayexpress

Arp2/3 Complex Activity Enables Nuclear YAP for Naïve Pluripotency of Human Embryonic Stem Cells

Project description:Our understanding of transitions of human embryonic stem cells between distinct stages of pluripotency relies predominantly on regulation by transcriptional and epigenetic programs with limited insight on the role of established morphological changes. We report remodeling of the actin cytoskeleton of human embryonic stem cells (hESCs) as they transition from primed to naïve pluripotency that includes assembly of a ring of contractile actin filaments encapsulating colonies of naïve hESCs. Activity of the Arp2/3 complex is required for the actin ring, uniform cell mechanics within naïve colonies, nuclear translocation of the Hippo pathway effectors YAP and TAZ, and effective transition to naïve pluripotency. RNA-sequencing analysis confirms that Arp2/3 complex activity regulates Hippo signaling in hESCs, and impaired naïve pluripotency with inhibited Arp2/3 complex activity is rescued by expressing a constitutively active, nuclear-localized YAP-S127A. Moreover, expression of YAP-S127A partially restored in actin filament fence with Arp2/3 complex inhibition, suggesting that actin filament remodeling is both upstream and downstream of YAP activity. These new findings on the cell biology of hESCs reveal a mechanism for cytoskeletal dynamics coordinating cell mechanics to regulate gene expression and facilitate transitions between pluripotency states.

2024-09-11 | GSE276968 | GEO

Project description:Comparative Transcriptome Analysis of PTCs

| PRJEB21364 | ENA

Niche stiffening compromises stem cell potential during aging by reducing chromatin accessibility at bivalent promoters

Project description:Tissue homeostasis and regeneration require activation and subsequent lineage commitment of tissue-resident stem cells (SCs). These state changes are controlled by epigenetic barriers. Using hair follicle stem cells (HFSCs) as paradigm, we studied how aging impacts the chromatin landscape and function of mammalian SCs. Analyses of genome-wide chromatin accessibility revealed that aged HFSCs displayed widespread reduction of chromatin accessibility specifically at key SC self-renewal and differentiation genes that were characterized by bivalent promoters carrying both activating and repressive chromatin marks. Consistently, aged HFSCs showed reduced self-renewing capacity and attenuated ability to activate expression of these bivalent genes upon regeneration. These functional defects were niche-dependent as transplantation of aged HFSCs into young recipients or into ex vivo niches restored SC functions and transcription of poised genes. Mechanistically, aged HFSC niche displayed wide-spread alterations in extracellular matrix composition and mechanics, resulting in compressive forces on SCs and subsequent transcriptional repression, leading to loss of bivalent promoters. Tuning tissue mechanics both in vivo and in vitro recapitulated age-related SC changes, implicating niche mechanics as a central regulator of genome organization and function leading to age-dependent SC exhaustion.

2021-05-07 | PXD018352 | Pride

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