Abstract
Over sixty percent of all mammalian protein-coding genes are estimated to be regulated by microRNAs (miRNAs), and unsurprisingly miRNA dysregulation has been linked with cancer. Aberrant miRNA expression in cancer cells has been linked with tumourigenesis and drug resistance. In the past decade, increasing number of studies have demonstrated that cholesterol accumulation fuels tumour growth and contributes to drug resistance, therefore, miRNAs controlling cholesterol metabolism and homeostasis are obvious hypothetical targets for investigating their role in cholesterol-mediated drug resistance in cancer. In this review, we have collated published evidences to consolidate this hypothesis and have scrutinized it by utilizing computational tools to explore the role of miRNAs in cholesterol-mediated drug resistance in breast cancer cells. We found that hsa-miR-128 and hsa-miR-223 regulate genes mediating lipid signalling and cholesterol metabolism, cancer drug resistance and breast cancer genes. The analysis demonstrates that targeting these miRNAs in cancer cells presents an opportunity for developing new strategies to combat anticancer drug resistance.
Highlights
MiRNAs are small non-coding RNAs (20-22 nucleotides) [1] found to be present in animals and plants [2], of which some are conserved in bilaterian organisms.[3]
We found that hsa-miR-128 and hsa-miR-223 regulate genes mediating lipid signalling and cholesterol metabolism, cancer drug resistance and breast cancer genes
We explored the possibility of miRNAs to be involved in cholesterol-mediated cancer drug resistance
Summary
MiRNAs are small non-coding RNAs (20-22 nucleotides (nt)) [1] found to be present in animals and plants [2], of which some are conserved in bilaterian organisms.[3]. Www.Genes&Cancer.com hsa-miR-128 and hsa-miR-223 potentially regulate genes involved in cholesterol-mediated drug resistance in breast cancer Altered expression was found in all target genes of hsa-miR-128 and hsamiR-223 compared to the normal tissue samples, which mediate breast cancer, drug resistance and lipoprotein and www.Genes&Cancer.com cholesterol signalling (Figure 3).
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