ArticleCancer gene therapy2024
AMIGO2 enhances the invasive potential of colorectal cancer by inducing EMT.
Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- AMIGO2 as a Novel Biomarker Predicting Poor Prognosis and Associated with Adhesion-Driven Metastasis in Pancreatic Adenocarcinoma.International journal of medical sciences · 2026Article
- AMIGO2 accelerates tumor progression by inducing a cancer stem cell-like phenotype.Scientific reports · 2025Article
- AMIGO2 expression at the invasive front of bladder cancer predicts recurrence-free and overall survival after radical cystectomy.Oncology letters · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
In our previous studies, we identified amphoterin-inducible gene and open reading frame 2 (AMIGO2) as a driver gene for liver metastasis and found that AMIGO2 expression in cancer cells worsens the prognosis of patients with colorectal cancer (CRC). Epithelial-mesenchymal transition (EMT) is a trigger for CRC to acquire a malignant phenotype, such as invasive potential, leading to metastasis. However, the role of AMIGO2 expression in the invasive potential of CRC cells remains unclear. Thus, this study aimed to examine AMIGO2 expression and elucidate the mechanisms by which it induces EMT and promotes CRC invasion. Activation of the TGFβ/Smad signaling pathway was found involved in AMIGO2-induced EMT, and treatment with the TGFβ receptor inhibitor LY2109761 suppressed AMIGO2-induced EMT. Studies using CRC samples showed that AMIGO2 expression was highly upregulated in the invasive front, where AMIGO2 expression was localized to the nucleus and associated with EMT marker expression. These results suggest that the nuclear translocation of AMIGO2 induces EMT to promote CRC invasion by activating the TGFβ/Smad signaling pathway. Thus, AMIGO2 is an attractive therapeutic target for inhibiting EMT and metastatic CRC progression.
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Registered trials
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