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¹ Human Cancer Genetics Program, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
² Division of Pathology, University of Rome ‘La Sapienza’, Ospedale Sant'Andrea, Rome, Italy

(Correspondence should be addressed to A Vecchione, Human Cancer Genetics Program, Division of Pathology, Comprehensive Cancer Center, The Ohio State University, 400 West 12th Avenue, Columbus, OH 43216, USA; Email: andrea.vecchione{at}uniroma1.it)

This paper is one of 6 papers that form part of a special Focus Section on microRNAs. The Guest Editors for this section were Professor Alfredo Fusco, Naples, Italy, and Professor Carlo M Croce, Columbus, OH, USA; they were not involved in the handling of this paper, on which they are listed as an author.

Apoptosis is a tightly regulated form of cell death and represents an important process during normal development. In the past years, the scientific community has produced remarkable advances in our understanding of cancer biology, realizing that apoptosis and the genes that control it have a profound effect on the malignant phenotype. Recently, a new class of non-coding RNA genes, known as microRNA (miRNA or miR), have been demonstrated to play important roles in diverse biological processes, including development, cell differentiation, proliferation, and apoptosis. This suggests that other oncogenic mechanisms are needed to produce selective pressure to override apoptosis during multistage carcinogenesis. Intriguingly, since most cytotoxic anticancer agents induce apoptosis, it is possible that defects in apoptotic programs may contribute to treatment failure. Several studies strongly suggest a role for microRNAs in modulating sensitive/resistant phenotypes to cytotoxic therapy, calling for further investigation and validation of microRNA functions and targets in order to improve sensitivity to cancer treatments, thus ultimately improving prognosis and survival. Here, we review the current findings about microRNAs focusing on their involvement in the apoptotic process.

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