4.5 Article

LGR6 Promotes Tumor Proliferation and Metastasis through Wnt/β-Catenin Signaling in Triple-Negative Breast Cancer

Journal

MOLECULAR THERAPY-ONCOLYTICS
Volume 18, Issue -, Pages 351-359

Publisher

CELL PRESS
DOI: 10.1016/j.omto.2020.06.020

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Funding

  1. National Natural Science Foundation of China [81672598]
  2. Science and Technology Planning Project of Guangzhou [201704020188]

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Leucine-rich-repeat-containing G protein-coupled receptor 6 (LGR6) has been identified as the stem cell marker in multiple normal tissues and malignancies. Previous studies implicated paradoxical functions of LGR6 as a tumor-suppressor gene or oncogene given to the specific context. To explore the exact role of LGR6 in triple-negative breast cancer (TNBC) that never has been studied before, in this study, we assessed LGR6 expression levels by RT-P CR and immunohistochemistry. LGR6 stable expressing/silenced cells were established, and functional assays on tumor proliferation, as well as metastasis, were conducted both in vitro and in vivo. Here, we found that LGR6 was overexpressed in TNBC, which correlated with poor disease-free and overall survivals. Functional assays both in vitro and in vivo showed that LGR6 promotes tumor proliferation and metastasis. LGR6 also increased the ability of tumor spheroid formation. Underlying mechanism exploration further revealed that the oncogenic role of LGR6 might be associated with the Wnt/beta-catenin pathway. In conclusion, our findings first proved that LGR6 acts as an oncogene in (TNBC), indicating that LGR6 might be a potential therapeutic target for TNBC treatment.

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