ArticleDrug development research2025
rFIP-GMI Suppresses IGF-1-Induced Invasion and Migration in Breast Cancer Cells via PI3K/Akt/β-Catenin Inhibition.
Article in Drug development research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Genetically predicted inflammatory cytokines mediate the associations between the gut microbiota and ovarian cancer: a bidirectional two-sample Mendelian randomization study.Journal of ovarian research · 2026Article
- rFIP-GMI Suppresses IGF-1-Induced Invasion and Migration in Breast Cancer Cells via PI3K/Akt/β-Catenin Inhibition.Drug development research · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Insulin-like growth factor-1 (IGF-I) promotes breast cancer (BC) progression by activating the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which enhances invasion and migration through β-catenin-mediated epithelial-mesenchymal transition (EMT). Triple-negative breast cancer (TNBC), an aggressive BC subtype lacking hormone receptors and HER2 expression, exhibits high metastatic potential, poor prognosis, and limited therapeutic options. The recombinant fungal immunomodulatory protein from Ganoderma microsporum (rFIP-GMI) possesses anti-inflammatory, anti-allergic, and anticancer activities; however, its role in suppressing tumor invasion and migration remains unclear. In this study, we investigated the molecular mechanism of rFIP-GMI in TNBC cell lines, Hs578T and MDA-MB-231. Cell invasion and migration were evaluated using Boyden chamber and Transwell migration assays, while Western blot analysis and nuclear/cytoplasmic fractionation were employed to analyze protein expression and β-catenin localization. rFIP-GMI significantly inhibited IGF-1-induced invasion and migration in both TNBC cell lines. Mechanistically, rFIP-GMI suppressed PI3K and Akt phosphorylation, thereby activating glycogen synthase kinase-3 beta (GSK3β) and promoting β-catenin phosphorylation and degradation. This led to reduced nuclear β-catenin accumulation and downregulation of oncogenic targets, including c-Myc, cyclin D1, and MMP-9. Conversely, treatment with the proteasome inhibitor MG132 confirmed that rFIP-GMI stabilized cytoplasmic β-catenin phosphorylation and blocked its nuclear translocation. Collectively, these findings demonstrate that rFIP-GMI inhibits IGF-1-driven invasion and migration in TNBC by inactivating the PI3K/Akt/β-catenin axis, highlighting its potential as a therapeutic agent for this aggressive TNBC subtype.
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Registered trials
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.