Grigorios Theodoropoulos1,*, Evangelos Tsiambas2,6*, Paraskevi Tziakou3*, Despoina Spyropoulou4*, Athanasios Niotis5, Harikleia Gakiopoulou6, Odysseas Dimas7, Loukas Manaios8, Andreas C Lazaris6, Georgia Thomopoulou9

1Department of Urology, “Elpis” General Hospital, Athens, Greece.

2Department of Cytology, 417 VA (NIMTS), Athens, Greece.

3Department of Pathology, “Thriasio” General Hospital, Elefsina, Greece.

4Department of Radiation Oncology, Medical School, University of Patras, Greece.

5Department of Surgery, 417 VA (NIMTS), Athens, Greece.

6Department of Pathology, Medical School, University of Athens, Greece.

72nd Department of Internal Medicine, ‘’Gennimatas’’ General Hospital, Athens, Greece.

8Department of Surgery, Bioclinic Medical Center, Athens, Greece.

9Department of Cytopathology, University General Hospital “Attikon’’, Athens, Greece.

*These authors contributed equally to this work

Epithelial malignancies demonstrate aggressive phenotypes (increased metastatic potential) due to mechanisms including the epithelial-to-mesenchymal transition (EMT). Novel micro-epigenetic markers –the micro-RNAs (miRs) – are under investigation in solid malignancies for diagnostic, prognostic or specific targeted therapy purposes. miRs are considered very promising and significant genetic markers for categorizing patients by their molecular characteristics, extending also their complicated genetic signatures. miRs are short, non-coding RNAs consisting of 20-25 nucleotides located at intra- or inter-gene regions. Functional miRs mediate a positive regulation of posttranscriptional gene silencing. Their deregulation in cancer cells due to genetic (mutations, translocations), epigenetic (DNA hypermethylation of tumour suppressor genes, extensive genomic DNA hypomethylation, aberrant histone modification patterns) and transcriptional alterations leads to a loss of miRs-mediated repression of target mRNA. Interestingly, a biphasic role of miRs in cancers of different histogenetic origin has been confirmed. In some of them, their upregulation correlates with an increased ongogenic activity, whereas in others the same miR type acts as a suppressor agent. In the current special molecular review we describe specific miRs in EMT development and progression in renal cell carcinoma (RCC).

Key words: gene, renal cell carcinoma, microRNAs, epithelial-to-mesenchymal transition.

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