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Fibroblast-Derived Thrombospondin 2 Shapes the Immune-Exclusionary Environment at Invasive Fronts in Colorectal Cancer [RNA-seq_Mouse_Tumor]

ABSTRACT: Fibrotic colorectal cancers (CRC) are characterized by immune exclusion driven by activated stroma, particularly by cancer-associated fibroblasts (CAFs). We identified that the matricellular protein thrombospondin-2 (THBS2) is highly expressed in the stroma of fibrotic CRCs. We performed orthotopic implantation of CMS4-like mouse tumor organoid (MTO) into WT and Thbs2 KO mice. Tumors developed in Thbs2 KO mice were considerably smaller and exhibited increased CD8 T cell infiltration and higher numbers of apoptotic tumor cells compared with WT mice. Our aim is to elucidate how Thbs2 in tumor microenvironment influences tumor growth.

ORGANISM(S): Mus musculus

PROVIDER: GSE285501 | GEO | 2025/10/28

REPOSITORIES: GEO

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Fibroblast-Derived Thrombospondin 2 Shapes the Immune-Exclusionary Environment at Invasive Fronts in Colorectal Cancer [scRNA-seq]

Project description:Fibrotic colorectal cancers (CRC) are characterized by immune exclusion driven by activated stroma, particularly by cancer-associated fibroblasts (CAFs). We identified that the matricellular protein thrombospondin-2 (THBS2) is highly expressed in the stroma of fibrotic CRCs. We performed orthotopic implantation of CMS4-like mouse tumor organoid (MTO) into WT and Thbs2 KO mice. Tumors developed in Thbs2 KO mice were considerably smaller and exhibited increased CD8 T cell infiltration and higher numbers of apoptotic tumor cells compared with WT mice. Our aim is to elucidate how Thbs2 in tumor microenvironment influences tumor growth.

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Fibroblast Derived Thrombospondin-2 Shapes the Immune-Exclusionary Environment at Invasive Fronts in Colorectal Cancer [RNA-seq_Mouse_CAF]

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Fibroblast-Derived Thrombospondin 2 Shapes the Immune-Exclusionary Environment at Invasive Fronts in Colorectal Cancer [RNA-seq_Human_CRC]

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Fibroblast-Derived Thrombospondin 2 Shapes the Immune-Exclusionary Environment at Invasive Fronts in Colorectal Cancer [Visium

Project description:Fibrotic colorectal cancers (CRC) are characterized by immune exclusion driven by activated stroma, particularly by cancer-associated fibroblasts (CAFs). This study aims to describe characteristics of spatial immune landscape of CRCs, which are subtyped by transcriptomic signatures and microsatellite instability.

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Proteome Profiling Identifies Markers for Inflammation-Related Tumor-Fibroblast Interaction in Colorectal Cancer

Project description:Inflammation has been identified as an important factor in cancer development and progression, including colorectal cancer [CRC]. To determine the role of inflammation and the specific contribution of activated fibroblasts in cancer development and progression we analyzed six human CRC tissue specimens and paired normal adjacent mucosa samples by LS/MS-MS. Amongst other, indeed several inflammation associated proteins were found differentially expressed compared to normal colonic mucosa. Two candidate molecules, SPARC and THBS2 were recently identified as proteins of a fibroblast inflammation signature. Analysis of public available RNA expression datasets revealed, that the mRNA of both SPARC and THBS2 are upregulated in CRC, typically in association with the CRC consensus molecular subtype 4 [CMS4]. Immunohistochemistry staining also demonstrated upregulation of SPARC and THBS2 in the tumor stroma compared to normal adjacent mucosa and indicated co-localization with the mesenchymal marker [alpha]SMA. In vitro 3D co-culture experiments with human colon derived fibroblasts and CRC cell lines resulted in enhanced SPARC and THBS2 protein levels when both cell types were cultivated in direct physical contact, compared to fibroblasts or cancer cells alone. This study demonstrates the feasibility of detecting tumor-specific signatures by LC-MS/MS and compatibility with RNA expression datasets. We identified an inflammation signature in CRC tissue and the data emphasized the contribution of activated fibroblasts in these events.

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Transcription profiling of mouse control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte)

Project description:The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92).<br>In this experiment we compare the gene expression profiles between a control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte). CMS4-met cells were injected iv. to the mouse tails. Three days later, either saline or tumor-specific CTL were injected iv into mouse tails. Single cell suspensions were made from mouse lungs and put in culture. Tumor cells were recovered from cultures. Tumor cells established from mice receiving saline were termed CMS4-met.cntl. Tumor cells established from mice receiving CTL were termed CMS4-met.sel. The gene expression profiles of these two tumor cell lines were then compared to CMS4-met.

2005-05-08 | E-MEXP-287 | biostudies-arrayexpress

Transcription profiling of in vivo-derived CMS4-met cells and the in vitro-derived CMS4.sel cells using CMS4 cells as a reference sample

Project description:The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92). The CMS4.sel subline was selected from the parental line in vitro following six successive passages in the presence of anti-Fas stimuli as described (Liu K, Abrams SI. Alterations in Fas expression are characteristic of, but not solely responsible for, enhanced metastatic competence. J Immunol 2003;170:5973-80).<br>In this experiment we compare the gene expression patterns of the in vivo-derived CMS4-met cells and the in vitro-derived CMS4.sel cells using CMS4 cells as a reference sample.

2005-05-08 | E-MEXP-286 | biostudies-arrayexpress