ArticleBritish journal of cancer2013
Silencing NOTCH signaling causes growth arrest in both breast cancer stem cells and breast cancer cells.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.
- Pooled it
- Psoralidin inhibits stemness-associated characteristics in cervical cancer cells via modulation of Oct4/Sox2 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Phytochemical basis and antitumor mechanisms ofFrontiers in immunology · 2026Review
- Natural product derived phytochemicals as modulators of cancer stemness and drug resistance.Frontiers in oncology · 2026Review
- Lp‑PLA2 in the cancer landscape: From molecular mechanisms to therapeutic potential (Review).International journal of oncology · 2025Review
- Protein Marker-Dependent Drug Discovery Targeting Breast Cancer Stem Cells.International journal of molecular sciences · 2025Review
- Cancer stem cells: landscape, challenges and emerging therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Article
- Notch and Hedgehog Signaling Unveiled: Crosstalk, Roles, and Breakthroughs in Cancer Stem Cell Research.Life (Basel, Switzerland) · 2025Review
- Review
- Recent Insights Into Breast Cancer: Molecular Pathways, Epigenetic Regulation, and Emerging Targeted Therapies.Breast cancer : basic and clinical research · 2025Review
- ALDHCells · 2024Article
- Inhibition of Cancer Stem-like Cells by Curcumin and Other Polyphenol Derivatives in MDA-MB-231 TNBC Cells.International journal of molecular sciences · 2024Article
- C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer.Nature communications · 2024Article
- Targeting Cervical Cancer Stem Cells by Phytochemicals.Current medicinal chemistry · 2024Review
- A Notch signaling-related lncRNA signature for predicting prognosis and therapeutic response in clear cell renal cell carcinoma.Scientific reports · 2023Article
- Psoralidin inhibits osteosarcoma growth and metastasis by downregulating ITGB1 expression via the FAK and PI3K/Akt signaling pathways.Chinese medicine · 2023Article
- In Vitro Evaluation of ALDH1A3-Affinic Compounds on Breast and Prostate Cancer Cell Lines as Single Treatments and in Combination with Doxorubicin.Current issues in molecular biology · 2023Article
- Re-Sensitizing Cancer Stem Cells to Conventional Chemotherapy Agents.International journal of molecular sciences · 2023Review
- A small molecule inhibitor of Notch1 modulates stemness and suppresses breast cancer cell growth.Frontiers in pharmacology · 2023Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer stem cells (BCSCs) are characterized by high aldehyde dehydrogenase (ALDH) enzyme activity and are refractory to current treatment modalities, show a higher risk for metastasis, and influence the epithelial to mesenchymal transition (EMT), leading to a shorter time to recurrence and death. In this study, we focused on examination of the mechanism of action of a small herbal molecule, psoralidin (Pso) that has been shown to effectively suppress the growth of BSCSs and breast cancer cells (BCCs), in breast cancer (BC) models.
methodsALDH(-) and ALDH(+) BCCs were isolated from MDA-MB-231 cells, and the anticancer effects of Pso were measured using cell viability, apoptosis, colony formation, invasion, migration, mammosphere formation, immunofluorescence, and western blot analysis.
resultsPsoralidin significantly downregulated NOTCH1 signaling, and this downregulation resulted in growth inhibition and induction of apoptosis in both ALDH(-) and ALDH(+) cells. Molecularly, Pso inhibited NOTCH1 signaling, which facilitated inhibition of EMT markers (β-catenin and vimentin) and upregulated E-cadherin expression, resulting in reduced migration and invasion of both ALDH(-) and ALDH(+) cells.
conclusionTogether, our results suggest that inhibition of NOTCH1 by Pso resulted in growth arrest and inhibition of EMT in BCSCs and BCCs. Psoralidin appears to be a novel agent that targets both BCSCs and BCCs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.