**1. Introduction**

Gene silencing by RNA occurs when dsRNA induces cleavage of its complementary mRNA, which is known as RNA interference (RNAi). RNA interference (RNAi) is the mechanism that suppresses gene expression or translation through the activity of RNA interference molecules (RNAi), by the neutralization of mRNA molecules. RNAi is also part of the cell's endogenous

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biological defense system which protects it against transposons and viruses. miRNAs and siRNAs are vital players in driving RNA interference mechanisms. These small RNAs bind mRNA molecules and either decrease or increase their activity and preventing their translation into protein.

In addition to RNAi, studies have identified several endogenous small RNA types including- endogenous siRNA (endo-siRNA), small noncoding RNAs (miRNAs), and piwi-interacting RNA (piRNA) which has created a wider view of normal and pathological cellular mechanisms [1]. The above types are considered non-coding RNAs (ncRNAs) which describes any RNA that does not encode a protein [2, 3]. Since the early 1990s, ncRNAs including miRNAs and siRNAs have been the subject of intensive research. Although non-protein coding RNAs (ncRNAs) were first imagined as simply 'junk' RNA with no functional purpose, they have- emerged as potent gene silencing factors [4]. Despite the importance of miRNA in medicine, mechanisms of genes targeting, their interaction with other cellular RNAs, as well as their mRNA editing capabilities are not yet fully understood [5]. It is clear that, the role of ncRNAs in the regulation of genes renders them putative targets for the development of novel drug therapies. As effectors, siRNAs and miRNAs can be used to silence or 'switch- off' specific cancer genes. Thus, gene silencing via RNA interference (RNAi) is evolving as- an aspect of cancer chemotherapy that could be personalized for individual patients. The therapeutic potential of miRNAs and siRNAs to play a key role in the treatment of cancer and other genetic diseases has been extensively investigated [2]. With the aim of mitigating side effects on healthy tissue, recent approaches have involved the selective targeting of- mutant cancer cells.

At present, the main hurdle in implementing miRNA and siRNA therapy in the clinic is the absence of an efficient and targeted delivery system that would protect ncRNAs from degradation by endogenous RNAses and permit them to reach the precise tumor target [6]. Recently, nanoparticle technology and breast cancer targeting immunoconjugates for the delivery of siRNAs and miRNAs were demonstrated to control breast cancer tumor growth and metastasis [7].

MicroRNAs (miRs) are genomically encoded small, non-coding, single stranded RNA 18–25 nucleotides that regulate gene expression during embryonic development. In normal cells they act as a delicate switch in regulating cellular functions such as cell proliferation and cell differentiation [6]. Various preclinical research studies have sought to establish diagnostic, prognostic and therapeutic uses for miRNAs [3]. As a result, downregulated miRNAs in cancer cells are referred to as tumor suppressor miRNAs, while miRNAs that permit the expression of genes involved in cancerous processes are called oncomiRs [1]. siRNAs (with 21–25 nucleotides) are produced from exogenous double stranded (dsRNA); their structure is closely related to that of mature miRNAs. Nevertheless, similarities in the mechanisms and biogenesis of siRNAs and miRNAs have been observed. For example, both depend on Dicer enzymes and on Ago proteins. Most miRNAs, for example, are excised from the precursor (pre-miRNAs) by Dicer while the Ago will support the silencing [8].
