Abstract
Acquisition of drug resistance leads to failure of anti-cancer treatments and therapies. Although several successive chemotherapies are available, along with efforts towards clinical applications of new anti-cancer drugs, it is generally realized that there is a long way to go to treat cancers. Resistance to anti-cancer drugs results from various factors, including genetic as well as epigenetic differences in tumors. Determining the molecular and cellular mechanisms responsible for the acquisition of drug resistance may be a helpful approach for the development of new therapeutic strategies to overcome treatment failure. Several studies have shown that the acquisition of drug resistance is tightly regulated by post-transcriptional regulators such as RNA binding proteins (RBPs) and microRNAs (miRNAs), which change the stability and translation of mRNAs encoding factors involved in cell survival, proliferation, epithelial-mesenchymal transition, and drug metabolism. Here, we review our current understanding of ribonucleoprotein complexes, including RBPs and miRNAs, which play critical roles in the acquisition of drug resistance and have potential clinical implications for cancer.
Highlights
Chemotherapy, using anti-cancer drugs, has been widely used in treatment of malignancies, primary or acquired drug resistance cause therapeutic failure in cancer treatment
Numerous studies have shown that post-transcriptional regulators, especially miRNAs, were differentially expressed and involved in the direct or indirect regulation of drug resistance, there is still a considerable lack of understanding of the detailed mechanisms and intracellular pathways regulated by RNA binding proteins (RBPs) and/or miRNAs
We discussed recent studies showing that ribonucleoprotein complexes, including RBPs and miRNAs, could play critical roles in the regulation of anti-cancer drug efficacy by regulating their target mRNA stability and translational efficiency
Summary
Chemotherapy, using anti-cancer drugs, has been widely used in treatment of malignancies, primary or acquired drug resistance cause therapeutic failure in cancer treatment. Accumulating evidence indicates that there are fine-tuning steps in the regulation of gene expression at the mRNA level [11] This is executed by post-transcriptional regulators, such as RNA binding proteins (RBPs) and miRNAs. In eukaryotic cells, all RNAs are associated with RBPs co-transcriptionally and form ribonucleoprotein (RNP) complexes, which are composed of, various proteins, and RNAs such as small nuclear RNAs (snRNAs) and miRNAs [12,13,14]. Differential expression or defects of RBPs are related to several human diseases such as neuropathies, muscular atrophies and cancers [16,17] Another post-transcriptional regulator miRNAs are small noncoding RNAs involved in the regulation of gene expression. We will review recent findings on post-transcriptional regulation of drug resistance-related genes by RNP complexes, including RBPs and miRNAs
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