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Epiregulin Promotes Lung Metastasis of Salivary Adenoid Cystic Carcinoma.


ABSTRACT: Salivary adenoid cystic carcinoma (SACC) is a peculiar malignant tumor, characterized by its slow but inexorable growth, with a high incidence of lung metastasis and poor prognosis. Here, we show the upregulated expression of EGFR ligand epiregulin in a subset of SACC cells correlates with lung metastasis and unfavorable outcome in patients with SACC. We found that upregulation of epiregulin in SACC cells induced epithelial-mesenchymal transition by regulating GLI1/E-cadherin. Elevated epiregulin increased the expression of pro-angiogenic factors, such as VEGFA, bFGF, and IL-8. We also show that epiregulin can be delivered via exosomes and was enriched in exosomes derived from epiregulin-overexpressing SACC cells. Furthermore, treating immunodeficient mice with these epiregulin-enriched exosomes greatly enhanced SACC metastasis to lung. These epiregulin-enriched exosomes significantly enhanced angiogenesis in the neighboring tumor microenvironment and increased vascular permeability in the pre-metastatic lung microenvironment in vivo. Therefore, epiregulin, as well as epiregulin-containing exosomes, may be a novel target for controlling SACC lung metastasis.

SUBMITTER: Yang WW 

PROVIDER: S-EPMC5667342 | biostudies-other | 2017

REPOSITORIES: biostudies-other

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Epiregulin Promotes Lung Metastasis of Salivary Adenoid Cystic Carcinoma.

Yang Wen-Wen WW   Yang Lin-Qian LQ   Zhao Fei F   Chen Chu-Wen CW   Xu Li-Hua LH   Fu Jia J   Li Sheng-Lin SL   Ge Xi-Yuan XY  

Theranostics 20170823 15


Salivary adenoid cystic carcinoma (SACC) is a peculiar malignant tumor, characterized by its slow but inexorable growth, with a high incidence of lung metastasis and poor prognosis. Here, we show the upregulated expression of EGFR ligand epiregulin in a subset of SACC cells correlates with lung metastasis and unfavorable outcome in patients with SACC. We found that upregulation of epiregulin in SACC cells induced epithelial-mesenchymal transition by regulating GLI1/E-cadherin. Elevated epireguli  ...[more]

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