Chen-Ying Liu1,2*, Ajaybabu V. Pobbati2, Zhenyu Huang1, Long Cui1 and Wanjin Hong2
1 Department of Colorectal and Anal Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
2 Institute of Molecular and Cell Biology, Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive, Proteos, Singapore 138673, Singapore
Published in Cancer Res. 2017 Sep 1;77(17):4734-4735. Published first August 15, 2017.
Transglutaminase 2 (TG2) is a multifunctional protein that is overexpressed in multiple cancers and its expression levels positively correlate with metastasis and poor prognosis. Interestingly, TG2 is an activator of NF-kB and is also a direct target of NF-kB. It has been shown that knockdown of TG2 inhibits YAP activity. Here, in various cell lines, we show that TG2 is a direct target of YAP/TAZ; by upregulating TG2 expression, YAP/TAZ probably also forms a positive-feedback loop and amplifies oncogenic programs. TG2 has been a promising therapeutic target for many diseases, including cancer. Our results suggest that inhibition of TG2 could be a potent therapeutic strategy for the YAP/TAZ-active cancers.
Figure legend: Analysis of Cancer Cell Line Encyclopedia (CCLE) microarray dataset reveals that the mRNA expression of TG2 correlates well with the known YAP/TAZ target genes and YAP/TAZ mRNA levels. The co-expression data was extracted from the cBioportal database. The values of Pearson’s correlation and Spearman’s correlation were generated and used for evaluating the significance of co-expression by the cBioportal.
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