Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA96371 | ENA |
REPOSITORIES: ENA
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Project description:Analyze TGF-beta pathway transcriptional regulation in breast cancer stem cells with different responses upon TGF-beta pathway activation. Total RNA from four breast cell lines grown as mammospheres treated with recombinant TGF-beta or a TGF-beta receptor I inhibitor was used in the analysis.
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Project description:Transforming growth factor (TGF)-β signaling is a key driver to induce epithelial-to-mesenchymal transition (EMT), a process that enhances cancer cell plasticity and metastatic potential. However, the role of circular RNAs (circRNAs) in TGF-β signaling remains largely unexplored. Here, we identify circTBRII(3-6), a circRNA derived from TGF-β type II receptor (TBRII) pre-mRNA, as a critical enhancer of TGF-β/SMAD signaling in breast cancer cells. Depletion of circTBRII(3-6) inhibits TGF-β-induced EMT, migration, and in vivo extravasation of breast cancer cells. Mechanistically, circTBRII(3-6) acts as a scaffold that facilitates the interaction between the RNA-binding protein insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) and TGF-β type I receptor (TBRI) mRNA in an N6-methyladenosine (m6A)-dependent manner, and thereby stabilizes TBRI and promotes its expression. Furthermore, IGF2BP3 knockdown reduces circTBRII(3-6)-mediated enhancement of TGF-β/SMAD signaling, as well as TGF-β-induced EMT and migration. Our findings identify circTBRII(3-6) as a novel enforcer of TGF-β/SMAD signaling at the receptor level and highlight IGF2BP3 as a critical m6A reader that mediates circTBRII(3-6)-driven breast cancer cell plasticity.
2026-04-27 | PXD061218 | Pride
Project description:Transforming growth factor-β (TGF-β) comprises a key component in the tumor microenvironment. It is reported that TGF-β can be pro-tumorigenic or anti-tumorigenic depending on various contexts. Some of the triple negative breast cancers highly express TGF-β, but pro-tumorigenic function of TGF-β in triple negative breast cancer cells is not fully known. Therefore, we analyzed genome-wide gene expression changes after stimulation with TGF-β in a triple negative breast cancer cell line, Hs578T cells.
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Project description:Cancer Associated Fibroblasts (CAF) are a dominant and critical cell type of the tumour microenvironment and can lead to breast cancer progression. TGF-β has been reported to influence fibroblast to myofibroblast activation, which is similar to cancer associated fibroblast phenotype. To understand the mechanism of TGF-β mediated CAF phenotype, we have performed a comparative proteomic analysis of conditioned media from CAF (isolated from breast cancer biopsy tissues) and normal mammary fibroblasts engineered to over-express TGF-β1. Liquid chromatography/ tandem mass spectrometry (LC ESI Q-TOF-MS/MS) assay of conditioned media and Venn analysis of the acquired data, revealed approximately 185 common proteins secreted by the three fibroblast types (CAF, normal mammary fibroblasts and TGF-β over expressing mammary fibroblasts). Among these, 12 proteins exclusively overlap between normal fibroblasts and CAF and 20 proteins exclusively overlap between CAF and TGF-β1 over-expressing fibroblasts. This analysis reveals interesting targets which may be important in activation phenotype of CAF and breast cancer progression.
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Project description:TGF-betas have complex roles in tumorigenesis, with context-dependent effects that can either suppress or promote tumor progression. Our goal was to use integrated genomic approaches in a model of human breast cancer progression to identify core TGF-beta-regulated genes that specifically reflect the tumor suppressor activity of TGF-beta. The model consisted of the non-tumorigenic MCF10A (“M1”), the premalignant MCF10AT1k.cl2 (“M2”), the early malignant MCF10Ca1h (“M3”) and the highly malignant, metastatic MCF10Ca1a.cl1 (“M4”) cell lines. We have previously shown that tumor suppressor activity of TGF-beta is dependent on Smad3, and is lost in M4 cells. To identify how TGF-beta/Smad3 targets change with cancer progression, we performed promoter-wide Smad3 ChIP-chip on all four cell lines of the breast cancer progression model (M1-M4), following treatment with TGF-beta or vehicle control.
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Project description:TGF-beta signature in cholangiocarcinoma cell lines
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Project description:Transforming growth factor (TGF)-β signaling is a key driver to induce epithelial-to-mesenchymal transition (EMT), a process that enhances cancer cell plasticity and metastatic potential. However, the role of circular RNAs (circRNAs) in TGF-β signaling remains largely unexplored. Here, we identify circTGFBR2(3-6), a circRNA derived from TGF-β receptor 2 (TGFBR2) pre-mRNA, as a critical enhancer of TGF-β/SMAD signaling in breast cancer cells. Depletion of circTGFBR2(3-6) inhibits TGF-β-induced EMT, migration, and in vivo extravasation of breast cancer cells. Mechanistically, circTGFBR2(3-6) acts as a scaffold that facilitates the interaction between the RNA-binding protein insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) and TGF-β receptor 1 (TGFBR1) mRNA in an N6-methyladenosine (m6A)-dependent manner, and thereby stabilizes TGFBR1 and promotes its expression. Furthermore, IGF2BP3 knockdown reduces circTGFBR2(3-6)-mediated enhancement of TGF-β/SMAD signaling and TGF-β-induced EMT and migration. Our findings identify circTGFBR2(3-6) as a novel enforcer of TGF-β/SMAD signaling at the receptor level and highlight IGF2BP3 as a critical m6A reader that mediates circTGFBR2(3-6)-driven breast cancer cell plasticity.
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