miRNA (miR) are endogenous, small, singlestranded, ncRNAs that play important roles in multiple cellular processes [1], and are evolutionarily conserved in sequence between distantly related organisms, suggesting they are essential biomolecules. miRs act as negative regulators of gene expression at the post-transcriptional level, through binding to partially complementary sequence motifs present mainly in the 3 -UTRs of corresponding mRNAs, thereby causing either translational repression and/or target mRNA degradation. Recently it has been reported that conserved miR binding sites also exist in the open reading frame and 5 -UTR regions of target mRNAs [2]. There is a ‘many-to-many relationship’ between miRs and mRNAs with potential phenotypic consequences, as a single miR can simultaneously deregulate multiple mRNAs, while a single mRNA can be targeted by several miRs [3]. Since their discovery in 1993, there has now been a ‘miR revolution’ in molecular oncology and most human cancers have been profiled and classified by distinctive miR signatures. Alterations in miR expression and function contribute to cancer development through a multitude of mechanisms and miRs are able to act as tumor suppressors (TSG-miRs) or oncogenes (onco-miRs) in a tissue/tumor specific manner [4]. From this, the diagnostic value and therapeutic potential of miRs has been realized. Chemotherapy is widely used in the treatment of various types of cancer and adequate response is crucial for prolonging patient survival and improving quality of life. Despite the development of novel anticancer agents, drug resistance frequently hampers successful treatment and many tumors are still refractory to chemotherapy. Chemoresistance can be classified as either intrinsic or acquired. The intrinsic type of resistance refers to factors already present (including a combination of genetic and