ArticleCell communication and signaling : CCS2024
Transcriptional responses to direct and indirect TGFB1 stimulation in cancerous and noncancerous mammary epithelial cells.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Intrinsic cellular heterogeneity directs divergent epithelial-to-mesenchymal transition outcomes.The FEBS journal · 2026Article
- Role of Klhl14 in senescence and epithelial-to-mesenchymal transition via TGF-β modulation.Cell death & disease · 2026Article
- Multi-omic analysis of the liver-breast axis reveals key hepatic mediators of breast cancer progression.Science China. Life sciences · 2026Review
- TGFβ enhances platelet-breast-cancer-cell interaction and promotes platelet aggregation.The FEBS journal · 2026Article
- A Trifluoromethyl Quinazoline Compound Regulates the Epithelial-Mesenchymal Transition of Prostatic Hyperplasia Cells by Inhibiting the Secretion of TGF-β1 in Stromal Cells.Current issues in molecular biology · 2025Article
- Multi-Level Profiling of MAPK-Associated Genes and MicroRNAs Uncovers Regulatory Networks in Breast Cancer Subtypes.International journal of molecular sciences · 2025Article
- Article
- Improvement of Menopausal Symptoms byFood science & nutrition · 2025Article
- EMT induction in normal breast epithelial cells by COX2-expressing fibroblasts.Cell communication and signaling : CCS · 2025Article
- Integration of single-cell RNA and bulk RNA sequencing revealed malignant ductal cell heterogeneity and prognosis signatures in pancreatic cancer.Frontiers in immunology · 2025Article
- Molecular crossroads: identifying MAPK proteins bridging SMAD and dopamine pathways in breast cancer.Cell cycle (Georgetown, Tex.)Article
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9 authors.
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Abstract
backgroundTransforming growth factor beta (TGFβ) is important for the morphogenesis and secretory function of the mammary gland. It is one of the main activators of the epithelial-mesenchymal transition (EMT), a process important for tissue remodeling and regeneration. It also provides cells with the plasticity to form metastases during tumor progression. Noncancerous and cancer cells respond differently to TGFβ. However, knowledge of the cellular signaling cascades triggered by TGFβ in various cell types is still limited.
methodsMCF10A (noncancerous, originating from fibrotic breast tissue) and MCF7 (cancer, estrogen receptor-positive) breast epithelial cells were treated with TGFB1 directly or through conditioned media from stimulated cells. Transcriptional changes (via RNA-seq) were assessed in untreated cells and after 1-6 days of treatment. Differentially expressed genes were detected with DESeq2 and the hallmark collection was selected for gene set enrichment analysis.
resultsTGFB1 induces EMT in both the MCF10A and MCF7 cell lines but via slightly different mechanisms (signaling through SMAD3 is more active in MCF7 cells). Many EMT-related genes are expressed in MCF10A cells at baseline. Both cell lines respond to TGFB1 by decreasing the expression of genes involved in cell proliferation: through the repression of MYC (and the protein targets) in MCF10A cells and the activation of p63-dependent signaling in MCF7 cells (CDKN1A and CDKN2B, which are responsible for the inhibition of cyclin-dependent kinases, are upregulated). In addition, estrogen receptor signaling is inhibited and caspase-dependent cell death is induced only in MCF7 cells. Direct incubation with TGFB1 and treatment of cells with conditioned media similarly affected transcriptional profiles. However, TGFB1-induced protein secretion is more pronounced in MCF10A cells; therefore, the signaling is propagated through conditioned media (bystander effect) more effectively in MCF10A cells than in MCF7 cells.
conclusionsEstrogen receptor-positive breast cancer patients may benefit from high levels of TGFB1 expression due to the repression of estrogen receptor signaling, inhibition of proliferation, and induction of apoptosis in cancer cells. However, some TGFB1-stimulated cells may undergo EMT, which increases the risk of metastasis.
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