AMIGO2

Last update 23 Jan 2025

Basic Info

Synonyms

adhesion molecule with Ig like domain 2, ALI1, Alivin-1

+ [5]

Introduction

Required for depolarization-dependent survival of cultured cerebellar granule neurons. May mediate homophilic as well as heterophilic cell-cell interaction with AMIGO1 or AMIGO3. May contribute to signal transduction through its intracellular domain. May be required for tumorigenesis of a subset of gastric adenocarcinomas.

100 Clinical Results associated with AMIGO2

100 Translational Medicine associated with AMIGO2

0 Patents (Medical) associated with AMIGO2

102

Literatures (Medical) associated with AMIGO2

01 Jan 2025·The Journal of Pathology

AMIGO2 characterizes cancer‐associated fibroblasts in metastatic colon cancer and induces the release of paracrine active tumorigenic secretomes

Article

Author: Naschberger, Elisabeth ; Petter, Katja ; Yong, Yongsong ; Zhou, Yonghua ; Gass, Tobias ; Demmler, Richard ; Zohud, Bisan Abdalfatah ; Merkel, Susanne ; Zhang, Tong ; Schellerer, Vera S ; Stürzl, Michael ; Fang, Qi ; Geppert, Carol I ; Flierl, Christian

AbstractSecretomes of cancer‐associated fibroblasts (CAFs) in colorectal cancer (CRC) contribute to malignancy. Detailed knowledge is available on the components and functions of CAF secretomes. Little is known about the regulation of CAF secretomes. Here, we searched for receptor‐like membrane‐bound molecules in CAFs, which may regulate the production and release of tumor‐activating secretomes. The adhesion molecule with Ig‐like domain 2 (AMIGO2) was significantly upregulated in cultivated CAFs compared to normal tissue‐associated fibroblasts (NAFs), and this was confirmed in patient‐derived tissues. AMIGO2 expression was low or absent in healthy colon, significantly increased in fibroblasts of primary CRC, and highest in the stromal tissues of CRC‐derived liver metastases. AMIGO2 expression in CAFs correlated with a higher T‐category, increased lymph node metastasis, progressed tumor stages and was associated with reduced survival in different cohorts of CRC patients. Interestingly, AMIGO2 expression was induced by transforming growth factor‐β and higher in female patients, who exhibit a more aggressive disease course. In functional studies, conditioned media of NAFs with experimentally induced AMIGO2 overexpression enhanced proliferation and migration of different CRC tumor cells, while siRNA‐mediated inhibition of AMIGO2 in CAFs attenuated these effects. Accordingly, therapeutic inhibition of the receptor‐like AMIGO2 protein in CRC CAFs could prevent tumorigenic secretomes in CRC. © 2024 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

02 Dec 2024·Cancer Discovery

A Targetable Secreted Neural Protein Drives Pancreatic Cancer Metastatic Colonization and HIF1α Nuclear Retention

Article

Author: Takahashi, Mai ; Tavazoie, Sohail F. ; Mei, Wenbin ; de Stanchina, Elisa ; Wu, Y. Gloria ; Hsu, Dennis ; Ravetch, Ethan ; Hayashi, Akimasa ; Lorenz, Ivo C. ; Umeda, Shigeaki ; Yamaguchi, Norihiro ; Iacobuzio-Donahue, Christine A. ; Khan, Abdul G.

AbstractPancreatic ductal adenocarcinoma (PDAC) is an increasingly diagnosed cancer that kills 90% of afflicted patients, with most patients receiving palliative chemotherapy. We identified neuronal pentraxin 1 (NPTX1) as a cancer-secreted protein that becomes overexpressed in human and murine PDAC cells during metastatic progression and identified adhesion molecule with Ig-like domain 2 (AMIGO2) as its receptor. Molecular, genetic, biochemical, and pharmacologic experiments revealed that secreted NPTX1 acts cell-autonomously on the AMIGO2 receptor to drive PDAC metastatic colonization of the liver—the primary site of PDAC metastasis. NPTX1–AMIGO2 signaling enhanced hypoxic growth and was critically required for hypoxia-inducible factor-1α (HIF1α) nuclear retention and function. NPTX1 is overexpressed in human PDAC tumors and upregulated in liver metastases. Therapeutic targeting of NPTX1 with a high-affinity monoclonal antibody substantially reduced PDAC liver metastatic colonization. We thus identify NPTX1–AMIGO2 as druggable critical upstream regulators of the HIF1α hypoxic response in PDAC.Significance: We identified the NPTX1–AMIGO2 axis as a regulatory mechanism upstream of HIF1α-driven hypoxia response that promotes PDAC liver metastasis. Therapeutic NPTX1 targeting outperformed a common chemotherapy regimen in inhibiting liver metastasis and suppressed primary tumor growth in preclinical models, revealing a novel therapeutic strategy targeting hypoxic response in PDAC.

01 Dec 2024·Cancer Gene Therapy

AMIGO2 enhances the invasive potential of colorectal cancer by inducing EMT

Article

Author: Hamada, Jun-ichi ; Sato, Reo ; Izutsu, Runa ; Okada, Futoshi ; Seong, HeeKyung ; Osaki, Mitsuhiko ; Ogata, Sanami ; Hamada, Jun-Ichi

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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AMIGO2

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