The extracellular matrix protects Bacillus subtilis colonies from Pseudomonas invasion and modulates plant co-colonization
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA483214 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7613014_1.fastq.gz | Fastqsanger.gz | |||
| SRR7613014_2.fastq.gz | Fastqsanger.gz | |||
| SRR7613015_1.fastq.gz | Fastqsanger.gz | |||
| SRR7613015_2.fastq.gz | Fastqsanger.gz | |||
| SRR7613016_1.fastq.gz | Fastqsanger.gz |
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| S-EPMC6478825 | biostudies-literature
Project description:We report the application of a high-throughput technique, RNA-seq, to study the transcriptomic response of P. chlororaphis and Bacillus subtilis growing in co-cultures in solid medium
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Project description:Background: Melanoma brain metastases (MBM) continues to be a significant clinical problem with limited treatment options. Highly invasive melanoma cells migrate along the vasculature and perivascular cells may contribute to residual disease and recurrence. PTEN loss and hyperactivation of AKT occur in MBM; however, a role for PTEN/AKT in perivascular invasion has not been described. Methods: We used in vivo intracranial injections of murine melanoma and bulk RNA sequencing of melanoma cells co-cultured with brain endothelial cells (brECs) to investigate brain colonization and perivascular invasion. Results: We found that PTEN-null melanoma cells were highly efficient at colonizing the perivascular niche relative to PTEN-expressing counterparts. PTEN re-expression (PTEN-RE) in melanoma significantly reduced brain colonization and migration along the vasculature. We hypothesized this phenotype was mediated through vascular-induced TGFβ secretion, which drives AKT phosphorylation. Disabling TGFβ signaling in melanoma cells reduced colonization and perivascular invasion; however, introduction of constitutively-active myristolated-AKT (myrAKT) restored overall tumor size but not perivascular invasion. Conclusions: PTEN loss facilitates perivascular brain colonization and invasion of melanoma. TGFβ-AKT signaling partially contributes to this phenotype, but further studies are needed to determine the complementary mechanisms that enable melanoma cells to both survive and spread along the brain vasculature.
2023-12-26 | GSE247232 | GEO
Project description:The extracellular matrix (ECM) plays a central role in regulating tumor progression and metastatic colonization by providing biochemical and mechanical signals that shape cancer cell fate. However, most organoid culture systems rely on basement membrane extracts that fail to reproduce the tissue-specific extracellular environments encountered during metastasis. Here, we develop tissue-derived decellularized matrix hydrogels to reconstruct organ-specific microenvironments and investigate epigenetic adaptation to ECM cues during metastatic colonization. Patient-derived colorectal cancer organoids cultured in colon-derived matrices exhibited enhanced maintenance of stem-like phenotypes and colon-specific chromatin accessibility landscapes compared with cultures grown in basement membrane extracts, demonstrating improved physiological relevance for primary tumor modeling. When exposed to matrices derived from secondary organs, the organoids showed distinct growth phenotypes accompanied by rapid, tissue-dependent chromatin accessibility remodeling, indicating that ECM composition alone can reshape regulatory programs governing metastatic adaptation. Notably, liver-derived matrices selectively activated hepatocyte nuclear factor 4 alpha (HNF4A)–associated transcriptional networks and created a context-specific dependence on c-MET signaling for survival. Functional perturbation of HNF4A or c-MET signaling confirmed that both are required for organoid formation specifically within the liver matrix environment. Together, these findings establish tissue-derived matrix hydrogels as instructive bioactive materials that actively regulate cancer cell epigenetic states and reveal microenvironment-specific therapeutic vulnerabilities during early metastatic colonization.
2026-09-10 | GSE324972 | GEO
Project description:Brain metastasis is a dismal complication of cancer that hinges on the initial survival and outgrowth of disseminated cancer cells. To better understand these crucial early stages of brain metastatic colonization, we investigated two prevalent sources of cerebral relapse in the clinic, triple-negative breast cancer (TNBC) and HER2+ breast cancer (HER2BC). We elucidated distinctive early tumor architectures, physical and functional stromal interfaces, and autocrine growth programs employed by these two tumor types to colonize the brain. TNBC cells form extensive perivascular sheath colonies with diffusive contact with astrocytes and microglia. In striking contrast, heightened autonomous deposition of several extracellular matrix components prompts HER2BC cells to colonize the brain as compact, spheroidal colonies, segregating stromal cells to the periphery of the colony. Single-cell dissection of the spatially resolved tumor microenvironment (TME) reveals that brain metastases activate – to different degrees – the canonical stages of the disease-associated microglia (DAM) response previously defined in Alzheimer’s disease. Differential engagement of paracrine tumor-DAM signaling through the receptor AXL suggests specific pro-metastatic functions of the tumor architecture in both TNBC perivascular and HER2BC spheroidal colonies. Collectively, our findings illuminate the distinct stereospatial features of two different yet highly efficient modes of brain colonization, and the relevance of these features in future efforts to leverage the TME to treat brain metastasis.
2023-05-02 | GSE223351 | GEO
Project description:Brain metastasis is a dismal complication of cancer that hinges on the initial survival and outgrowth of disseminated cancer cells. To better understand these crucial early stages of brain metastatic colonization, we investigated two prevalent sources of cerebral relapse in the clinic, triple-negative breast cancer (TNBC) and HER2+ breast cancer (HER2BC). We elucidated distinctive early tumor architectures, physical and functional stromal interfaces, and autocrine growth programs employed by these two tumor types to colonize the brain. TNBC cells form extensive perivascular sheath colonies with diffusive contact with astrocytes and microglia. In striking contrast, heightened autonomous deposition of several extracellular matrix components prompts HER2BC cells to colonize the brain as compact, spheroidal colonies, segregating stromal cells to the periphery of the colony. Single-cell dissection of the spatially resolved tumor microenvironment (TME) reveals that brain metastases activate – to different degrees – the canonical stages of the disease-associated microglia (DAM) response previously defined in Alzheimer’s disease. Differential engagement of paracrine tumor-DAM signaling through the receptor AXL suggests specific pro-metastatic functions of the tumor architecture in both TNBC perivascular and HER2BC spheroidal colonies. Collectively, our findings illuminate the distinct stereospatial features of two different yet highly efficient modes of brain colonization, and the relevance of these features in future efforts to leverage the TME to treat brain metastasis.
2023-05-02 | GSE223309 | GEO
Project description:Brain metastasis is a dismal complication of cancer that hinges on the initial survival and outgrowth of disseminated cancer cells. To better understand these crucial early stages of brain metastatic colonization, we investigated two prevalent sources of cerebral relapse in the clinic, triple-negative breast cancer (TNBC) and HER2+ breast cancer (HER2BC). We elucidated distinctive early tumor architectures, physical and functional stromal interfaces, and autocrine growth programs employed by these two tumor types to colonize the brain. TNBC cells form extensive perivascular sheath colonies with diffusive contact with astrocytes and microglia. In striking contrast, heightened autonomous deposition of several extracellular matrix components prompts HER2BC cells to colonize the brain as compact, spheroidal colonies, segregating stromal cells to the periphery of the colony. Single-cell dissection of the spatially resolved tumor microenvironment (TME) reveals that brain metastases activate – to different degrees – the canonical stages of the disease-associated microglia (DAM) response previously defined in Alzheimer’s disease. Differential engagement of paracrine tumor-DAM signaling through the receptor AXL suggests specific pro-metastatic functions of the tumor architecture in both TNBC perivascular and HER2BC spheroidal colonies. Collectively, our findings illuminate the distinct stereospatial features of two different yet highly efficient modes of brain colonization, and the relevance of these features in future efforts to leverage the TME to treat brain metastasis.
2023-05-02 | GSE223247 | GEO
Project description:Tissue-derived extracellular matrix hydrogels instruct epigenetic adaptation in metastatic colonization
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Project description:Bioluminescent Imaging Reveals Novel Patterns of Colonization and Invasion in Systemic Escherichia coli K1 Experimental Infection in the Neonatal Rat
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