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Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

ABSTRACT: We report the new role that the interaction of cells with the surrounding extracellular matrix can exert on the differnetiation patterns controlled by the BMP pathway. In cells bearing Apc mutations, modulation of this pathway triggers cells irresponsive to normal differentiation cues which offers a posible therapeutic anchor for anti-cancer therapies.

ORGANISM(S): Mus musculus

PROVIDER: GSE178856 | GEO | 2022/08/19

REPOSITORIES: GEO

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Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

Project description:Extracellular matrix interactions provide an escape mechanism for commitment to differentiation in cancer

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Identification of bone morphogenetic protein (BMP)-7 as a key instructive factor for human epidermal Langerhans cell differentiation and proliferation

Project description:Langerhans dendritic cells represent abundantly occuring and evolutionary highly conserved DCs specifically located in the stratified epithelial tissues. LCs are unique among DC family members in that they express epithelial-type adhesion molecules, allowing them to form a tight three-dimensional network in basal and suprabasal epidermal keratinocyte layers and developmentally dependent on the cytokine TGF-β1. In the present study, we identified BMP-7 as another key factor inducing LC differnetiation. Here we have performed comparative analysis of highly purified CD207+/CD1a+ in vitro generated Langerhans cells in the presence of BMP-7 and TGF-β1. We have identified that both BMP-7-LCs and TGF-β1-LCs are closely related to each other.

2013-10-18 | GSE49085 | GEO

Identification of bone morphogenetic protein (BMP)-7 as a key instructive factor for human epidermal Langerhans cell differentiation and proliferation

Project description:Langerhans dendritic cells represent abundantly occuring and evolutionary highly conserved DCs specifically located in the stratified epithelial tissues. LCs are unique among DC family members in that they express epithelial-type adhesion molecules, allowing them to form a tight three-dimensional network in basal and suprabasal epidermal keratinocyte layers and developmentally dependent on the cytokine TGF-M-NM-21. In the present study, we identified BMP-7 as another key factor inducing LC differnetiation. Here we have performed comparative analysis of highly purified CD207+/CD1a+ in vitro generated Langerhans cells in the presence of BMP-7 and TGF-M-NM-21. We have identified that both BMP-7-LCs and TGF-M-NM-21-LCs are closely related to each other. CD34+ hematopoietic stem cells were isolated from freshly obtained cord blood and cultured in the presence of GM-CSF, SCF, Flt3L, TNFa and either TGF-M-NM-21 or BMP-7 for 7 days to get immature LCs. RNA was isolated from these in vitro genetared LCs.

2013-10-18 | E-GEOD-49085 | biostudies-arrayexpress

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Project description:AUTS2 forms a novel complex to recruit CUL4 E3 for BMP inhibition and neural differnetiation

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Beclin1 Deficiency Unlocks Cardiac Lineage Commitment through Convergent Wnt and BMP Signaling Activation

Project description:Beclin1 plays significant roles in cardiac organogenesis. Beclin1 can regulate the fate conversion of fibroblasts into cardiomyocytes. However, the function and mechanism of Beclin1 in regulating early cardiac lineage commitment and differentiation remain unclear. To explore its potential role in cardiac lineage development, we utilized model of cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) to simulate early cardiogenesis and investigated the function of Beclin1. We show that the knockdown of Beclin1 facilitates cardiomyocyte differentiation. Through bulk RNA-sequencing analysis, we found that knocking down Beclin1 activated the Wnt signaling pathway at the embryoid body stage but inhibited its activity at the cardiomyocyte stage. Moreover, the Bone morphogenetic protein (Bmp) signaling pathway was continuously activated throughout cardiomyocyte differentiation process. Our findings demonstrate a novel function of Beclin1 during cardiac differentiation. The activation of Wnt-mediated Bmp signaling pathway represents a major mechanism by which the deficiency of Beclin1 promotes mESCs differentiation into cardiomyocytes.

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GPI-anchored Timp1 protein

Project description:Tissue inhibitor of metalloproteinase 1 (TIMP-1) controls matrix metalloproteinase (MMP) activity through 1:1 stochiometric binding. Human TIMP-1 fused to a glycosylphosphatidylinositol (GPI) anchor (TIMP-1-GPI) shifts the activity of TIMP-1 from the extracellular matrix to the cell surface. TIMP-1-GPI treated renal cell carcinoma cells (RCC) show increased apoptosis and reduced proliferation. Transcriptomic profiling and regulatory pathway mapping were used to identify potential mechanisms driving these effects. Significant changes in inhibitor of DNA binding (IDs), TGF-β1/SMAD and BMP pathways resulted from TIMP-1-GPI treatment. These events were linked to reduced TGF-β1 signaling mediated by inhibition of proteolytic processing of latent TGF-β1 by TIMP-1-GPI. Activity of TIMP-1 from the extracellular matrix to the cell surface. TIMP-1-GPI treated renal cell carcinoma cells (RCC) show increased apoptosis and reduced proliferation. Transcriptomic profiling and regulatory pathway mapping were used to identify potential mechanisms driving these effects. Significant changes in inhibitor of DNA binding (IDs), TGF-β1/SMAD and BMP pathways resulted from TIMP-1-GPI treatment. These events were linked to reduced TGF-β1 signaling mediated by inhibition of proteolytic processing of latent TGF-β1 by TIMP-1-GPI. Renal cell carcinoma cells were transfected with empty vector, rhTimp1 and 2 concentrations of Timp1-GPI fusion protein

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Spatial control of the APC/C ensures the rapid degradation of Cyclin B1

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Project description:The goal of this study is to compare next-generation sequencing-derived osteoblast transcriptome profilings to identify essential genes during isteoblast differnetiation.

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| PRJNA385861 | ENA