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EMP1 regulates cell proliferation, migration, and stemness in gliomas through PI3K‐AKT signaling and CD44
Author(s) -
Wang Junxiang,
Li Xuetao,
Wu Haibin,
Wang Hao,
Yao Lin,
Deng Zhitong,
Zhou Youxin
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28974
Subject(s) - glioma , cd44 , cancer research , pi3k/akt/mtor pathway , gene silencing , protein kinase b , biology , pathology , signal transduction , cell , microbiology and biotechnology , medicine , gene , biochemistry , genetics
Glioblastoma multiforme (GBM) is an intracranial tumor; the feature is higher malignant and poorer prognosis. The search for therapeutic targets for gliomas has always been a focus of research in the field of neurology. The unusual expression of epithelial membrane protein 1 (EMP1) has been proved in most tumors. In our study, we determined the expression level of EMP1 expression in glioma tissues. There were higher levels of EMP1 in glioma tissues—particularly GBM tissues—than those in normal brain tissues. Then we discovered that silencing EMP1 inhibited glioma cell invasion and proliferation through inhibiting the PI3K‐AKT signaling pathway. Subsequently, we investigated the function of EMP1 on glioma stem cells and found that it regulates the expression of CD44 in such cells to promote stemness. Taken together, the new strategies for the treatment of glioma may be provided by these finding, thereby improving the prognosis associated with it.