Research

miR-21: an oncomir on strike in prostate cancer

Marco Folini^1* , Paolo Gandellini^1* , Nicole Longoni¹ , Valentina Profumo¹ , Maurizio Callari¹ , Marzia Pennati¹ , Maurizio Colecchia² , Rosanna Supino¹ , Silvia Veneroni¹ , Roberto Salvioni³ , Riccardo Valdagni⁴ , Maria Grazia Daidone¹ and Nadia Zaffaroni¹

¹  Department of Experimental Oncology and Molecular Medicine, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian, 1, Milan, 20133, Italy

²  Department of Pathology, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian, 1, Milan, 20133, Italy

³  Department of Urology, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian, 1, Milan, 20133, Italy

⁴  Prostate Program, Scientific Directorate, Fondazione IRCCS Istituto Nazionale dei Tumori, Via Venezian, 1, Milan, 20133, Italy

author email corresponding author email* Contributed equally

Molecular Cancer 2010, 9:12doi:10.1186/1476-4598-9-12

Published:	21 January 2010

Abstract

Background

Aberrant expression of microRNAs, small non-coding RNA molecules that post-transcriptionally repress gene expression, seems to be causatively linked to the pathogenesis of cancer. In this context, miR-21 was found to be overexpressed in different human cancers (e.g. glioblastoma, breast cancer). In addition, it is thought to be endowed with oncogenic properties due to its ability to negatively modulate the expression of tumor-suppressor genes (e.g. PTEN) and to cause the reversion of malignant phenotype when knocked- down in several tumor models. On the basis of these findings, miR-21 has been proposed as a widely exploitable cancer-related target. However, scanty information is available concerning the relevance of miR-21 for prostate cancer. In the present study, we investigated the role of miR-21 and its potential as a therapeutic target in two prostate cancer cell lines, characterized by different miR-21 expression levels and PTEN gene status.

Results

We provide evidence that miR-21 knockdown in prostate cancer cells is not sufficient per se i) to affect the proliferative and invasive potential or the chemo- and radiosensitivity profiles or ii) to modulate the expression of the tumor-suppressors PTEN and Pdcd4, which in other tumor types were found to be regulated by miR-21. We also show that miR-21 is not differently expressed in carcinomas and matched normal tissues obtained from 36 untreated prostate cancer patients subjected to radical prostatectomy.

Conclusions

Overall, our data suggest that miR-21 is not a central player in the onset of prostate cancer and that its single hitting is not a valuable therapeutic strategy in the disease. This supports the notion that the oncogenic properties of miR-21 could be cell and tissue dependent and that the potential role of a given miRNA as a therapeutic target should be contextualized with respect to the disease.