ArticleCancer cell international2024
Inhibition of ABI2 ubiquitination-dependent degradation suppresses TNBC cell growth via down-regulating PI3K/Akt signaling pathway.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Systematic AI-assisted screening of the cadhesome to map epithelial monolayer mechanics.Cell communication and signaling : CCS · 2026Article
- TRIM32-mediated ABI2 downregulation promotes anoikis resistance and metastasis by regulating EMT in lung adenocarcinoma.Cellular and molecular life sciences : CMLS · 2026Article
- Piezoelectric cold atmospheric plasma modulates neurogenic cell proliferation and differentiation via cross-signaling.IBRO neuroscience reports · 2026Article
- Mechanism of Morbidity Based on Ulcerative Colitis: A Review of Traditional Chinese Medicine Treatment of Ulcerative Colitis.International journal of general medicine · 2025Review
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10 authors.
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Abstract
Triple negative breast cancer (TNBC) is a type of cancer that lacks receptor expression and has complex molecular mechanisms. Recent evidence shows that the ubiquitin-protease system is closely related to TNBC. In this study, we obtain a key ubiquitination regulatory substrate-ABI2 protein by bioinformatics methods, which is also closely related to the survival and prognosis of TNBC. Further, through a series of experiments, we demonstrated that ABI2 expressed at a low level in TNBC tumors, and it has the ability to control cell cycle and inhibit TNBC cell migration, invasion and proliferation. Molecular mechanism studies proved E3 ligase CBLC could increase the ubiquitination degradation of ABI2 protein. Meanwhile, RNA-seq and IP experiments indicated that ABI2, acting as a crucial factor of tumor suppression, can significantly inhibit PI3K/Akt signaling pathway via the interaction with Rho GTPase RAC1. Finally, based on TNBC drug target ABI2, we screened and found that FDA-approved drug Colistimethate sodium(CS) has significant potential in suppressing the proliferation of TNBC cells and inducing cell apoptosis, making it a promising candidate for impeding the progression of TNBC.
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