TAZ plays an important role in the progression of breast and non-small cell lung cancer. Importantly, TAZ confers cancer stem cell-related traits on breast cancer cells, its importance in tumor initiation and progression. TAZ is also overexpressed in papillary thyroid carcinoma. TAZ and YAP have been shown to interact with several transcriptional factors, with the TEAD family of transcriptional factors being the most relevant in cell proliferation and cancer progression. The X-ray crystal structures of YAP-TEAD complexes have been resolved and the proposed interaction is supported by and consistent with functional analysis, showing that YAP-TEAD complexes activates gene transcription. YAP expression was observed in colon adenocarcinoma. It is overexpressed in human colon cancer specimens and overexpression of YAP promotes cell proliferation and survival in colon cancer cells. Recent findings show that knockdown of TAZ results in a decrease in cell proliferation in culture and tumor growth in vivo. Despite evidence suggesting the potential implication of YAP and TAZ in colon cancer progression, their prognostic significance in colorectal cancer is unknown. In this study, we analyzed the mRNA expression of YAP and TAZ, and two of its downstream target genes, AXL and CTGF, in two independent colon cancer patient cohorts comprising 522 patients. We found that TAZ, but not YAP, is a prognostic marker in colon cancer progression. Furthermore, TAZ-AXL-CTGF co-overexpression, which defines both the expression of TAZ and its transcriptional activity on target gene expression, is a novel prognostic indicator, that is independent of tumor grade and stage, for colon cancer patients. The role of TAZ in colon cancer cell proliferation and oncogenesis was validated by functional study. The top 20 small molecules were further analyzed Albaspidin-AA through a Pubmed search regarding their effects on treatment of colon cancer. We found that amiloride and tretinoin have yielded 55 and 123 publications, respectively, when coupled with colon cancer in the search engine. Several publications have shown their inhibitory effect on colon cancer growth. Amiloride treatment has been shown to inhibit the growth of colon cancer cells in vitro and in vivo. Importantly, it can sensitize 
doxorubicin resistant colon cancer cells to treatment with doxorubicin, suggesting that amiloride and doxorubicin can be combined to treat doxorubicin resistant colon cancer. Tretinoin, also known as alltrans retinoic acid, has been shown to inhibit proliferation and anchorage-independent growth of colon cancer cells in vitro and in vivo, probably through regulating the differentiation state of cancer cells. In the present study, we have shown that TAZ mRNA expression is positively correlated with two of its downstream targets, AXL and CTGF, and that TAZ is significantly associated with poor survival of colon cancer patients in two independent colon cancer datasets, comprising 522 patients. Interestingly, the upregulation of AXL and CTGF, which reflects the increased transcriptional activity of TAZ-TEAD complexes, can be used in combination with TAZ mRNA expression, for better prognostification in these two independent colon cancer patient datasets. Genes that are co-regulated with TAZ-AXL-CTGF overexpression are involved in several important cellular processes, including cell migration, angiogenesis and calcium signaling, as well as others that have already been Pimozide described as prognostic markers for colon cancer progression. These genes may be upstream factors or downstream effectors of TAZ and the dysregulated Hippo pathway in colon cancers.