We propose that FGFR2 IIIb overexpression

We propose that FGFR2 IIIb overexpression new enhances cancer cells’ ability to interact with and become dependent on paracrine stimulation by mesenchymal-derived FGF ligands. Such hypothesis will need further investigation and be validated in other cancer types. We plan to investigate the relevance of these potential predictive biomarkers in ongoing pancreatic cancer clinical trials using dovitinib at our institution (ClinicalTrials.gov ID NCT01497392). Acknowledgments The studies were supported by internal institutional funding. Notes The authors declare no conflict of interest. Footnotes Supplementary Information accompanies this paper on British Journal of Cancer website (http://www.nature.com/bjc) Supplementary Material Supplementary Figures Click here for additional data file.(3.

3M, ppt) Supplementary Figures Legend Click here for additional data file.(36K, doc)
The first event in cancer metastasis is the movement of cancer cells away from the primary tumour tissue. Thereafter, cancer cells invade surrounding tissues and intravasate into vessels. Several reports have shown that the invasive capability of cancer cells is acquired by transformation to the mesenchymal phenotype (the epithelial-mesenchymal transition (EMT; Nieto, 2011). Moreover, EMT may produce cancer stemness properties (Alison et al, 2011). Inducers such as TWIST1, (Kang and Massague, 2004) SNAI1, (Pena et al, 2009) ZEB1, and ZEB2 (Chua et al, 2007) are reported to be associated with EMT in cancer cells. Most recently, Ocana et al (2012) reported that a newly identified EMT inducer, paired related homoeobox 1 (PRRX1), promoted full EMT in cancer cells.

However, they focused on the mesenchymal-to-epithelial transition (MET; Thiery et al, 2009) They showed that the loss of PRRX1 was required for cancer metastasis. Downregulation of PRRX1 caused the acquisition of MET. Low PRRX1 expression levels were significantly associated with metastasis and poor prognosis in the analysis of clinical samples of breast cancer and lung squamous cell carcinoma. Furthermore, the stemness phenotype was suppressed by PRRX1-induced EMT, and PRRX1 had to be downregulated to activate stem cell properties and allow colonisation. These findings were clearly distinct from previous analyses of EMT and the stemness phenotype. We noted that the function of PRRX1 in colorectal cancer (CRC) cells had not been elucidated.

Thus, the Entinostat purpose of the present study was to verify that PRRX1 induced EMT in CRC cells. We also examined the clinical significance of PRRX1 in CRC cases. Materials and methods Patients and sample collection A total of 173 CRC samples were obtained during surgery. All patients underwent resection of the primary tumour at Kyushu University Beppu Hospital and affiliated hospitals between 1992 and 2007.

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