Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176422 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:TGF-beta and BMP mediated gene expression in cultured sclerotome.
| PRJNA123819 | ENA
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.
2026-04-22 | GSE303132 | GEO
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.
2020-12-24 | GSE152414 | GEO
Project description:Transforming growth factor (TGF)-β signaling enhances cancer cell plasticity by inducing epithelial-to-mesenchymal transition (EMT). Here, we identified a TGF-β-induced long non-coding RNA, LIMD1 Antisense RNA 1 (LIMD1-AS1) that strengthens the SMAD-mediated transcriptional response to TGF-β. LIMD1-AS1 expression is upregulated in breast cancer tissues compared to normal breast tissues, and high LIMD1-AS1 expression is associated with poor prognosis in breast cancer patients. Depletion of LIMD1-AS1 hinders TGF-β-induced EMT, migration, and extravasation of breast cancer cells. Mechanistically, LIMD1-AS1 promotes the interaction between SMAD3 and its transcriptional coactivator p300, thereby enhancing SMAD3 transcriptional activity and TGF-β/SMAD signaling. We demonstrated that LIMD1-AS1 binds to the MAD homology 2 (MH2) domain of SMAD3 and the interferon-binding domain (IBiD) of p300. Displacing LIMD1-AS1 from p300 by its competitor interferon regulatory factor 3 (IRF3) suppressed the effects of LIMD1-AS1 on potentiating TGF-β/SMAD signaling. Furthermore, blockage of p300 acetyltransferase activity with a pharmacological inhibitor A-485 reduced the ability of LIMD1-AS1 to enhance SMAD3 transcriptional activity, TGF-β-induced EMT, and migration. This study identifies LIMD1-AS1 as a novel stimulator of TGF-β signaling by establishing a positive feedback loop and highlights its potential as a therapeutic target for breast cancer.
2025-07-08 | GSE288909 | GEO
Project description:Epithelial-to-mesenchymal transition (EMT) plays a crucial role in metastasis, which is the leading cause of death in breast cancer patients. We show that Cdc42 GTPase-activating protein (CdGAP) promotes tumor formation and metastasis to lungs in the HER2-positive (HER2+) murine breast cancer model. CdGAP facilitates intravasation, extravasation, and growth at metastatic sites. CdGAP depletion in HER2+ murine primary tumors mediates crosstalk with a Dlc1-RhoA pathway and is associated with a transforming growth factor-β (TGF-β)-induced EMT transcriptional signature. To further delineate the molecular mechanisms underlying the pro-migratory role of CdGAP in breast cancer cells, we searched for CdGAP interactors by performing a proteomic analysis using HEK293 cells overexpressing GFP-CdGAP. We found that CdGAP interacts with the adaptor Talin to modulate focal adhesion dynamics and integrin activation. Moreover, HER2+ breast cancer patients with high CdGAP mRNA expression combined with a high TGF-β-EMT signature are more likely to present lymph node invasion. Our results suggest CdGAP as a candidate therapeutic target for HER2+ metastatic breast cancer by inhibiting TGF-β and Integrin/Talin signaling pathways.
2023-07-14 | PXD043376 | Pride
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.
2025-08-26 | PXD022374 | Pride
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.
2012-02-09 | E-MTAB-516 | biostudies-arrayexpress
Project description:Transforming growth factor-β (TGF-β) is a key factor for the development of prostate cancer metastases in bone. In breast cancer and melanoma, studies have shown how TGF-β regulates gene expression to allow cancer cells to adapt to the bone microenvironment. We used microarray analyses to characterize the effect of TGF-β on gene expression in prostate cancer cells in vitro.
2014-11-01 | GSE58698 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature