ArticleExperimental & molecular medicine2015
β-TrCP1 degradation is a novel action mechanism of PI3K/mTOR inhibitors in triple-negative breast cancer cells.
Article in Experimental & molecular medicine, 2015. 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, 22 citations in OpenAlex.
- Decyl caffeate inhibits the proliferation of human triple negative breast cancer cells.BioMedicine · 2026Article
- JAK2 Inhibition Augments the Anti-Proliferation Effects by AKT and MEK Inhibition in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2025Article
- SMURF2 Facilitates GAP17 Isoform 1 Membrane Displacement to Promote Mutant p53-KRAS Oncogenic Synergy.Molecular cancer research : MCR · 2025Article
- Review
- Article
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- β-TrCP1 promotes cell proliferation via TNF-dependent NF-κB activation in diffuse large B cell lymphoma.Cancer biology & therapy · 2020Article
- Writing and erasing MYC ubiquitination and SUMOylation.Genes & diseases · 2019Review
- Prognostic values of F-box members in breast cancer: an online database analysis and literature review.Bioscience reports · 2019Review
- Novel chemotherapeutic agent, FND-4b, activates AMPK and inhibits colorectal cancer cell proliferation.PloS one · 2019Article
- MicroRNA-324-5p suppresses the migration and invasion of MM cells by inhibiting the SCFOncology letters · 2018Article
- Discovering new PI3Kα inhibitors with a strategy of combining ligand-based and structure-based virtual screening.Journal of computer-aided molecular design · 2018Article
- Review
- Triple negative breast cancer: shedding light onto the role of pi3k/akt/mtor pathway.Oncotarget · 2016Review
- Deubiquitinating c-Myc: USP36 steps up in the nucleolus.Cell cycle (Georgetown, Tex.) · 2015Article
- Circular RNA hsa_circ_0000376 Participates in Tumorigenesis of Breast Cancer by Targeting miR-1285-3p.Technology in cancer research & treatmentArticle
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
An F-box protein, β-TrCP recognizes substrate proteins and destabilizes them through ubiquitin-dependent proteolysis. It regulates the stability of diverse proteins and functions as either a tumor suppressor or an oncogene. Although the regulation by β-TrCP has been widely studied, the regulation of β-TrCP itself is not well understood yet. In this study, we found that the level of β-TrCP1 is downregulated by various protein kinase inhibitors in triple-negative breast cancer (TNBC) cells. A PI3K/mTOR inhibitor PI-103 reduced the level of β-TrCP1 in a wide range of TNBC cells in a proteasome-dependent manner. Concomitantly, the levels of c-Myc and cyclin E were also downregulated by PI-103. PI-103 reduced the phosphorylation of β-TrCP1 prior to its degradation. In addition, knockdown of β-TrCP1 inhibited the proliferation of TNBC cells. We further identified that pharmacological inhibition of mTORC2 was sufficient to reduce the β-TrCP1 and c-Myc levels. These results suggest that mTORC2 regulates the stability of β-TrCP1 in TNBC cells and targeting β-TrCP1 is a potential approach to treat human TNBC.
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