MiR-429 is linked to metastasis and poor prognosis in renal cell carcinoma by affecting epithelial-mesenchymal transition

Warning

This publication doesn't include Institute of Computer Science. It includes Central European Institute of Technology. Official publication website can be found on muni.cz.
Authors

MACHÁČKOVÁ Táňa MLČOCHOVÁ Hana STANIK Michal DOLEZEL Jan FEDORKO Michal PACÍK Dalibor POPRACH Alexandr SVOBODA Marek SLABÝ Ondřej

Year of publication 2016
Type Article in Periodical
Magazine / Source Tumor Biology
MU Faculty or unit

Central European Institute of Technology

Citation
Web http://link.springer.com/article/10.1007%2Fs13277-016-5310-9
Doi http://dx.doi.org/10.1007/s13277-016-5310-9
Field Oncology and hematology
Keywords Renal cell carcinoma; Epithelial-mesenchymal transition; microRNA; miR-429; E-cadherin
Attached files
Description MicroRNAs (miRNAs) have been proven to be important oncogenes and tumor suppressors in wide range of cancers, including renal cell carcinoma (RCC). In our study, we evaluated miRNA-429 as potential diagnostic/prognostic biomarker in 172 clear cell RCC patients and as a potential regulator of epithelial-mesenchymal transition (EMT) in vitro. We demonstrated that miR-429 is down-regulated in tumor tissue samples (P < 0.0001) and is significantly associated with cancer metastasis (P < 0.0001), shorter disease-free (P = 0.0105), and overall survival (P = 0.0020). In addition, ectopic expression of miR-429 in 786-0 RCC cells followed by TGF-beta treatment led to increase in the levels of E-cadherin expression (P < 0.0001) and suppression of cellular migration (P < 0.0001) in comparison to TGF-beta-treated controls. Taken together, our findings suggest that miR-429 may serve as promising diagnostic and prognostic biomarker in RCC patients. We further suggest that miR-429 has a capacity to inhibit loss of E-cadherin in RCC cells undergoing EMT and consequently attenuate their motility.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info