ArticleFrontiers in pharmacology2024
Parishin B blocking TRIB3-AKT1 interaction inhibits breast cancer lung metastasis.
Article in Frontiers in pharmacology, 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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Who cites it
4 citing papers in PubMed.
- Redefining breast cancer: therapeutic opportunities in HER2-low and emerging molecular subtypes.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Encapsulation of Protein-Based Drug Carriers for Controlled Loading and Releasing Efficiency: A Review.The protein journal · 2026Review
- Crotonoside exerts anti-colorectal cancer effects by suppressing KIF20A to regulate the cell cycle.Scientific reports · 2025Article
- Simultaneous Quantification of Multiple Analytes in Rat Plasma by UHPLC-MS/MS Following Oral Administration ofMolecules (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: TRIB3 has been reported to mediate breast cancer (BC) proliferation and metastasis by interacting with AKT1, and blocking the interaction between TRIB3 and AKT1 can inhibit the progression of BC. Besides, inhibiting TRIB3 to turn "cold tumor" hot has also been proved to be an effective therapeutic strategy for BC. Thus, this study aim to find drugs that can bind to TRIB3 to inhibit BC progression, and further elucidate its mechanism. Methods: The possible inhibitors of TRIB3 were screened by high-throughput molecular docking, CETSA, and CO-IP assay. Then, the effect of TRIB3 inhibitor anti BC was assessed by CCK-8 assay, flow cytometry, plate colony formation assay, and transwell assay; and the RNA-seq was empolyed to study the potential mechanism of Parishin B (PB) anti-BC. Finally, the effect of TRIB3 inhibitor on BC lung metastasis Results: PB was screened as a possible inhibitor of TRIB3, and CETSA and CO-IP assay indicated that PB could target TRIB3 and block TRIB3-AKT1 interaction. In addition, PB exhibited good anti-BC activity without drug toxicity in normal breast cells by experiments Conclusion: The study demonstrated PB can bind to TRIB3 to inhibit BC proliferation and lung metastasis by blocking TRIB3-AKT1 interaction and regulating cell cycle, providing a therapeutic agent for the treatment of BC.
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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 Socratic graph.