ArticleToxicological research2023
YPEL3 expression induces cellular senescence via the Hippo signaling pathway in human breast cancer cells.
Article in Toxicological research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Epithelial YPEL3 Modulates CD8Cancer science · 2026Article
- The multilayer coatings on polylactic acid implants spatiotemporally regulates the microenvironment to enhance antibacterial and osseointegration capacity.Materials today. Bio · 2026Article
- Pseudouridine synthases upregulate 5'-tRF-Lys to inhibit YPEL3 and drive malignant progression in nasopharyngeal carcinoma.Cellular & molecular biology letters · 2026Article
- Development and validation of an 11-CpG methylation signature-based nomogram for predicting prognosis in early-onset breast cancer.Translational cancer research · 2026Article
- Protein lactylation: molecular mechanisms underlying lactate-driven tumorigenesis and cancer progression.Cancer biology & therapy · 2025Review
- Canine mammary tumors as a promising adjunct preclinical model for human breast cancer research: similarities, opportunities, and challenges.Archives of pharmacal research · 2025Review
- Review
- Nuclear PD-L1 compartmentalization suppresses tumorigenesis and overcomes immunocheckpoint therapy resistance in mice via histone macroH2A1.The Journal of clinical investigation · 2024Article
- New Horizons in Cancer Progression and Metastasis:Biomedicines · 2024Review
- Upregulation of YPEL3 expression and induction of human breast cancer cell death by microRNAs.Toxicological research · 2024Article
- Enterococcus Phage vB_EfaS_HEf13 as an Anti-Biofilm Agent Against Enterococcus faecalis.Journal of microbiology (Seoul, Korea) · 2024Article
- Interactions between oxidative stress and senescence in cancer: Mechanisms, therapeutic implications, and future perspectives.Redox biology · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Hippo pathway is a signaling pathway that controls organ size in animals by regulating cell proliferation and apoptosis. Yes-associated protein 1 (YAP1), an oncogene associated with the development and progression of breast cancer, is downregulated by the Hippo pathway and is associated with the development and progression of breast cancer. Yippee-like 3 (YPEL3) is a target gene of the tumor suppressor protein p53, and its activation has been shown to inhibit cell growth, induce cellular senescence, and suppress tumor cell metastasis. In this study, we found that YAP1 inhibits the expression of YPEL3 expression in breast cancer cells. Furthermore, a decrease in lamin B1, a marker protein of cellular senescence, coupled with the activation of senescence-associated β-galactosidase indicated that upregulating YPEL3 levels through YAP1 downregulation can induce cellular senescence. Additionally, elevated YPEL3 levels resulted in higher levels of oxygen consumption rate in mitochondria, thus promoting apoptosis. This suggests that YPEL3 plays a crucial role in regulating oxidative stress and cell apoptosis in breast cancer cells. Therefore, the interaction between YAP1 and YPEL3 represents a novel mechanism of cellular senescence mediated by the Hippo signaling pathway. Collectively, our findings suggest that the Hippo signaling pathway plays an important role in regulating cellular senescence, which could have implications for the development of new therapeutic strategies for diseases such as cancer.
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