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Truncated TEAD‐binding protein of TAZ inhibits glioma survival through the induction of apoptosis and repression of epithelial‐mesenchymal transition
Author(s) -
Zhao Wei,
Li LiWen,
Tian RuiFeng,
Dong QiuFeng,
Li PengQi,
Yan ZhiFeng,
Yang Xin,
Huo JunLi,
Fei Zhou,
Zhen HaiNing
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.28997
Subject(s) - psychological repression , epithelial–mesenchymal transition , apoptosis , microbiology and biotechnology , transition (genetics) , mesenchymal stem cell , chemistry , cancer research , glioma , biology , gene , gene expression , biochemistry
Transcriptional coactivator with PDZ‐binding motif (TAZ), a Hippo pathway downstream effector, promotes tumor progression by serving as a transcriptional coactivator with TEAD. Here, we introduced a new construct which can express the TEAD‐binding domain of TAZ protein (TAZBD), and determined its antitumor effect in malignant glioma both in vitro and in vivo. We first observed that TAZ was upregulated in glioma tissues and related to malignant clinicopathologic characteristic, indicating the crucial role of TAZ during glioma progression. In U87 and U251 cells, TAZBD expression increased the proportion of apoptotic cells, and suppressed the colony formation and tumorigenicity. Further, TAZBD also decreased cell metastasis through the repression of epithelial‐mesenchymal transition. The mechanistic study showed that TAZBD suppression of glioma cells was predominantly through blocking the TAZ‐TEAD complex formation by competing with endogenous TAZ. Thus, the gene therapy of malignant glioma through blocking TAZ‐TEAD complex by TAZBD may provide a new way for the targeted therapy of glioma.