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Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [RNA-Seq]

ABSTRACT: Ameloblastoma is a locally aggressive odontogenic epithelial tumor with poorly understood intraosseous pathogenesis due to a lack of physiologically relevant models. Here, we established an orthotopic intraosseous mouse model using ameloblastoma epithelial cells in combination with ameloblastoma-derived mesenchymal stromal cells (AMMSCs) or their secretome. AMMSC-derived extracellular vesicle-enriched secretome enhances stemness, epithelial-mesenchymal transition (EMT) phenotypes, and tumorigenic ability of ameloblastoma epithelial cells. A unique signature of microRNAs in AMMSC-derived secretome is functionally associated with the upregulation of EMT-regulatory transcription factors in tumor epithelial cells. Single-nucleus ATAC and RNA sequencing revealed a dynamic EMT trajectory in primary human AM-derived epithelial cells activated by paired AMMSC-derived secretome. This study suggests that AMMSCs and their secretome drive orthotopic AM tumor development by promoting tumor epithelial cell proliferation, EMT, and vascular formation in the tumor microenvironment. This stromal-oriented orthotopic model provides a clinically relevant platform for dissecting tumor-stroma crosstalk and identifying therapeutic vulnerabilities in ameloblastoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE317372 | GEO | 2026/08/09

REPOSITORIES: GEO

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Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [multiome]

Project description:Ameloblastoma is a locally aggressive odontogenic epithelial tumor with poorly understood intraosseous pathogenesis due to a lack of physiologically relevant models. Here, we established an orthotopic intraosseous mouse model using ameloblastoma epithelial cells in combination with ameloblastoma-derived mesenchymal stromal cells (AMMSCs) or their secretome. AMMSC-derived extracellular vesicle-enriched secretome enhances stemness, epithelial-mesenchymal transition (EMT) phenotypes, and tumorigenic ability of ameloblastoma epithelial cells. A unique signature of microRNAs in AMMSC-derived secretome is functionally associated with the upregulation of EMT-regulatory transcription factors in tumor epithelial cells. Single-nucleus ATAC and RNA sequencing revealed a dynamic EMT trajectory in primary human AM-derived epithelial cells activated by paired AMMSC-derived secretome. This study suggests that AMMSCs and their secretome drive orthotopic AM tumor development by promoting tumor epithelial cell proliferation, EMT, and vascular formation in the tumor microenvironment. This stromal-oriented orthotopic model provides a clinically relevant platform for dissecting tumor-stroma crosstalk and identifying therapeutic vulnerabilities in ameloblastoma.

2026-08-09 | GSE317374 | GEO

Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [miRNA-Seq]

2026-08-09 | GSE317373 | GEO

Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [multiome]

Project description:Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [multiome]

| PRJNA1411998 | ENA

Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [RNA-Seq]

Project description:Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [RNA-Seq]

| PRJNA1412002 | ENA

Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [miRNA-Seq]

Project description:Stroma-oriented tumor microenvironment facilitates intraosseous ameloblastoma tumor growth [miRNA-Seq]

| PRJNA1412001 | ENA

Membrane-bound TGF-beta on tumor-associated mesenchymal stem-like cells initiates epithelial-to-mesenchymal transition in human colorectal cancer

Project description:Growing evidence indicates that tumor-associated stroma plays a negative role in human colorectal cancer (CRC). Nature of specific stromal cell populations involved and mechanisms underlying their negative impact remain to be fully understood. In this study we describe the expansion from human primary CRCs of a mesenchymal cell population, referred to as tumor-associated stromal cells (TASCs), resembling bone marrow-derived mesenchymal stem cells (BM-MSCs) in morphology, phenotypes and differentiation potential. We found that, upon co-culture with tumor cells, TASCs acquire membrane-bound TGF-mbTGF-expression, a phenomenon mediated by v6 integrin. MbTGF-expression proved to be critical for triggering epithelial-to-mesenchymal transition (EMT) in tumor cells, eventually leading to enhanced dissemination of circulating tumor cells and increased metastasis formation, in an orthotopic mouse model. Our data identify CRC-associated mesenchymal stem-like cells as critical EMT initiators and suggest mbTGF- as potential novel therapeutic target.

2022-05-19 | PXD005796 | Pride

Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis

Project description:The tumor microenvironment plays a critical role in cancer progression, but the precise mechanisms by which stromal cells influence the tumor epithelium are poorly understood. The signaling adapter p62 has been implicated as a positive regulator of epithelial tumorigenesis; however, its role in the stroma is unknown. We show here that p62 levels are reduced in the stroma of several tumors. Also, orthotopic and organotypic studies demonstrate that the loss of p62 in the tumor microenvironment or stromal fibroblasts resulted in increased tumorigenesis of epithelial prostate cancer cells. The mechanism involves the regulation of cellular redox through an mTORC1/c-Myc pathway of stromal glucose and amino acid metabolism. Inhibition of the pathway by p62 deficiency results in increased stromal IL-6 production, which is required for tumor promotion in the epithelial compartment. Thus, p62 is an anti-inflammatory tumor suppressor that acts through modulation of metabolism in the tumor stroma. C57BL6 syngeneic TRAMP-C2Re3 cells (5×10^4) were injected orthotopically into the prostate of WT (n=6) or p62 KO (n=6) mice (C57BL6 background) and tumor growth was assessed, followed by transcriptome profiling of the orthotopic tumors (n=12).

2014-07-23 | E-GEOD-55587 | biostudies-arrayexpress

Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [RNA-seq]

Project description:The Epithelial-to-Mesenchymal Transition (EMT) is a dynamic cellular program that is frequently used by cancer cells to increase migratory and invasive cell characteristics. It is a key contributor to both heterogeneity and chemo-resistance and metastasis in many solid tumors, including triple negative breast cancer. In particular, the intermediate or hybrid EMT state has increased tumor initiating and stem-like properties. Here, we have identified multiple distinct EMT states derived from the human breast cell line, SUM149PT, including three unique intermediate states, possessing distinct migratory, tumor initiating, and metastatic qualities. We have used this model to interrogate the epigenetic landscape of these distinct EMT states in a multi-omics approach, identifying and RUNX2 as relevant in regulating the intermediate state, as well as to develop a novel multiplexed staining approach to evaluate E-M heterogeneity (EMH) and overall EMT score in orthotopic tumors as well as patient tumor samples. This model reveals insights into the complex EMT spectrum of cell states, the networks that control them, and how EMT plasticity contributes to tumor heterogeneity in breast cancer.

2022-02-15 | GSE172609 | GEO

Phenotypic heterogeneity driven by plasticity of the intermediate EMT state governs disease progression and metastasis in breast cancer [ATAC-seq]

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Epithelial-to-Mesenchymal Transition of Murine PTEN-/- Liver Tumor Cells Promotes Tumor Growth and Invasion

Project description:Background: Epithelial-to-Mesenchymal Transition (EMT) is predicted to play a critical role in tumor progression and metastasis in Hepatocellular Carcinoma. Our goal was to elucidate a mechanism of tumor proliferation and metastasis using a novel murine model of EMT. Methods: 2Ã106 liver cells isolated from Ptenloxp/loxp;Alb-Cre+ mice, expanded from a single CD133+CD45- cell clone, Passage 0 (P0), were sequentially transplanted to obtain two passages of tumor cells, Passage 1 and 2 (P1 & P2) . Cells were analyzed for gene expression using microarray and real-time PCR. Functional analysis included cell proliferation, migration, and invasion in-vitro and orthotopic tumor growth and metastasis assays in-vivo. Results: Although P0, P1, and P2 each formed tumors consistent with mixed liver epithelium, within the P2 cells, two distinct cell types were clearly visible: cells with epithelial morphology similar to the P0 cells, and cells with fibroblastoid morphology. The P2 mesenchymal cells demonstrated increased locomotion on wound healing, increased cell invasion on Matrigel basement membrane, increased EMT associated gene Snail1, Zeb1, and Zeb2 expression, and down-regulated E-cadherin. P2 mesenchymal cells demonstrated significantly faster tumor growth compared to P2 Epithelial counterparts, with peritoneal seeding and invasion of intestine, pancreas, spleen, and lymph nodes. Furthermore, P2 mesenchymal cells secreted high levels of Hepatocyte Growth Factor (HGF), which acted in paracrine fashion to drive epithelial cells to undergo EMT. Conclusion: EMT is associated with a high rate of liver tumor proliferation, invasion, and metastasis in-vivo, which is driven by HGF in a feed-forward mechanism. Total RNA isolated from subcutaneously transplanted tumors with PTENloxp/loxp;Alb-Cre+ genetic background

2010-05-28 | E-GEOD-18255 | biostudies-arrayexpress

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