ArticleCell death & disease2022
RICH1 inhibits breast cancer stem cell traits through activating kinases cascade of Hippo signaling by competing with Merlin for binding to Amot-p80.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- Electroacupuncture enhances anti-tumor immunity in TNBC by reducing NE release and blocking α2-AR-mediated NGF/Hippo signaling.Chinese medicine · 2026Article
- Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.Molecular oncology · 2026Review
- GLUD1 supports ovarian cancer progression by counteracting anoikis via ARAF/MEK/ERK signaling.NPJ precision oncology · 2026Article
- RICH1 enhances pro-inflammatory TAM infiltration in breast cancer via promoting TRIM21-mediated ubiquitination of RhoA and inhibiting STAT3 phosphorylation.NPJ precision oncology · 2025Article
- ARHGAP17 Inhibits Hepatocellular Carcinoma Progression by Inactivation of Wnt/β-Catenin Signaling Pathway.Biochemical genetics · 2025Article
- ICOS-expressing CAR-T cells mediate durable eradication of triple-negative breast cancer and metastasis.Journal for immunotherapy of cancer · 2024Article
- Simultaneous screening of overexpressed genes in breast cancer for oncogenic drivers and tumor dependencies.Scientific reports · 2024Article
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
- RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2024Article
- Review
- ARHGAP44-mediated regulation of the p53/C-myc/Cyclin D1 pathway in modulating the malignant biological behavior of osteosarcoma cells.Journal of orthopaedic surgery and research · 2023Article
- Deciphering Common Traits of Breast and Ovarian Cancer Stem Cells and Possible Therapeutic Approaches.International journal of molecular sciences · 2023Review
- ARHGAP17 regulates the spatiotemporal activity of Cdc42 at invadopodia.The Journal of cell biology · 2023Article
- Tumor microenvironment enriches the stemness features: the architectural event of therapy resistance and metastasis.Molecular cancer · 2022Review
- The Hippo signalling pathway and its implications in human health and diseases.Signal transduction and targeted therapy · 2022Review
- Cytoskeletal and Cytoskeleton-Associated Proteins: Key Regulators of Cancer Stem Cell Properties.Pharmaceuticals (Basel, Switzerland) · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) are regarded as the root of tumor recurrence and distant metastasis, as well as the major cause of resistance to conventional cancer therapies. Elucidating the mechanism of regulating CSCs is of great significance for the development of CSCs-targeting therapy strategies. YAP/TAZ are identified as key regulators of CSCs-related traits on breast cancer cells; however, the upstream regulatory mechanism of Hippo kinases cascade involved in regulating YAP/TAZ remains elusive. In this study, we found that the low expression of RICH1 in breast cancer was associated with poor prognosis. Depletion of RICH1 promoted the stemness and disrupted the normal epithelial architecture of MCF10A cells. Besides, RICH1 inhibited the migration and invasion of breast cancer cells and sensitized these cells to chemotherapeutic drugs. Mechanistically, RICH1 activated the kinases cascade of Hippo signaling via displacing Amot-p80 from the complex with Merlin. Further studies revealed that the deletion of the BAR domain of RICH1 abolished the function of attenuating the binding of Amot-p80 and Merlin, illustrating that the competitive binding to Amot-p80 with Merlin was mediated by the BAR domain of RICH1. In conclusion, our work elucidated the role and molecular mechanism of RICH1 in stemness regulation of breast cancer, and might provide opportunities for CSCs-targeting therapy.
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