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Published in: Tumor Biology 7/2016

01-07-2016 | Original Article

SET7/9 inhibits oncogenic activities through regulation of Gli-1 expression in breast cancer

Authors: Yongchun Song, Jianli Zhang, Tao Tian, Xiao Fu, Wenjuan Wang, Suoni Li, Tingting Shi, Aili Suo, Zhiping Ruan, Hui Guo, Yu Yao

Published in: Tumor Biology | Issue 7/2016

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Abstract

SET7/9 is a protein lysine methyltransferase that had been initially identified as a histone lysine methyltransferase which generates monomethylation at histone 3 lysine 4. Different functions were attributed to the protein methylation mediated by SET7/9. In this study, we found that the expression of SET7/9 declined in a majority of the human breast cancer tissues examined compared with normal tissues. Knockdown of SET7/9 promoted the proliferation, migration, and invasion of breast cancer cells. Knockdown of SET7/9 also increased the tumorigenicity of breast cancer cells in vivo. On the contrary, overexpression of SET7/9 in breast cancer cells inhibited these processes. Microarray analysis indicated that Gli-1 may play function as a downstream factor of SET7/9. Overexpression of SET7/9SET7/9 inhibits Gli-1 expression. While knockdown of SET7/9 promotes the expression of Gli-1. Gli-1 inhibited by cyclopamine blocked knockdown SET7/9-driven proliferation, migration, and invasion in breast cancer cell. Furthermore, Gli-1 expression in human breast cancer tissues is negatively correlated with SET7/9 expression. Together, these results helped to realize the antioncogene functions of SET7/9 in breast cancer cells and provided a novel direction to treat breast cancer.
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Metadata
Title
SET7/9 inhibits oncogenic activities through regulation of Gli-1 expression in breast cancer
Authors
Yongchun Song
Jianli Zhang
Tao Tian
Xiao Fu
Wenjuan Wang
Suoni Li
Tingting Shi
Aili Suo
Zhiping Ruan
Hui Guo
Yu Yao
Publication date
01-07-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 7/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-016-4822-7

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