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TIMP4 expression is regulated by miR‐200b‐3p in prostate cancer cells
Author(s) -
Janiak Marek,
Paskal Wiktor,
Rak Beata,
Garbicz Filip,
Jarema Robert,
Sikora Krzysztof,
Włodarski Paweł
Publication year - 2017
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12638
Subject(s) - hyperplasia , prostate cancer , lncap , prostate , microrna , cancer research , cancer , adenocarcinoma , medicine , pca3 , transfection , biology , cell culture , gene , biochemistry , genetics
In prostate cancer TIMP 4 expression level fluctuates with tumor progression. The mechanism and factors influencing its expression remain unclear. The aim of the study was to test the hypothesis on regulation of TIMP 4 by micro RNA ‐200b‐3p. The levels of TIMP 4 and miR‐200b‐3p expression were determined by real time PCR in 27 prostate carcinomas and eight benign prostatic hyperplasia samples. We found that miR‐200b‐3p positively correlated with TIMP 4 expression in cancer samples (r = 0.46; p < 0.02). Moreover, mean miR‐200b‐3p level and TIMP 4 expression were both higher in cancer tissues compared to benign prostatic hyperplasia samples (p > 0.05). Next, to test probable mechanisms of the regulation androgen‐sensitive human prostate adenocarcinoma cells (LNCaP) were transfected with synthetic‐miR‐200b‐3p or its synthetic antagonist. Modulation of miR‐200b‐3p in LNC aP cells had an impact on TIMP 4 expression confirming the observation made in analyzed clinical samples. Two targets of miR‐200b‐3p: ZEB 1 and ETS 1 were investigated subsequently as potential regulators of TIMP 4, however, no effect of their modulation on TIMP 4 expression in LNC aP cells was found. Concluding, miR‐200b‐3p mediates regulation of TIMP 4 expression in prostate cancer but exact mechanism needs to be investigated.