Metabotropic Glutamate Receptor 8 Is Regulated by miR-33a-5p and Functions as an Oncogene in Breast Cancer
Author(s) -
Chunxu Zhang,
Shuang Xie,
Shou-Xin Yuan,
Yuanhao Zhang,
Yunhu Bai,
Lijia Chu,
Zuyin Wu,
Ninghui Guo,
Quanhui Wang,
Jixin Zhang
Publication year - 2021
Publication title -
journal of oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 54
eISSN - 1687-8469
pISSN - 1687-8450
DOI - 10.1155/2021/8002087
Subject(s) - oncogene , carcinogenesis , breast cancer , cancer research , medicine , flow cytometry , cancer , blot , cell growth , cell , cell cycle , ectopic expression , apoptosis , biology , immunology , cell culture , gene , biochemistry , genetics
It has been reported that glutamate metabotropic receptor 8 (GRM8) is closely implicated in the progression of human neuroblastoma, lung cancer, and glioma, but its role in breast cancer remains unknown. Thus, the present study was performed to uncover it. Immunohistochemistry, real-time PCR (RT-PCR), and western blotting experiments were performed to test GRM8 expression levels in tissues and cells. Cell functions were assessed by Cell Count Kit 8 (CCK-8), flow cytometry, wound healing, transwell chambers, and in vivo xenotransplantation experiments. The relationship between miR-33a-5p and GRM8 was evaluated by luciferase gene reporter and western blotting assay. The results showed that GRM8 expression was increased in breast cancer tissues and cells, which was closely associated with lower overall survival rate. Ectopic expression of GRM8 significantly enhanced cell growth, migration, and invasion and tumorigenesis and repressed cell apoptosis. In addition, GRM8 was under the negative regulation of miR-33a-5p, which was downregulated in breast cancer tissues and served as a tumor suppressor. Moreover, overexpression of GRM8 abrogated the inhibitive role of miR-33a-5p played in breast cancer. Collectively, this study reveals that GRM8 functions as an oncogene in breast cancer and is regulated by miR-33a-5p.
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