Abstract
The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.
Highlights
Cancer cells may initially respond to treatment, not all cells are eliminated
A recent study revealed that miR-488-3p levels are higher in cisplatin-resistant lung cancer cells than in parental cells, and nucleotide excision repair (NER) is activated by miR-488-3p, which targets Eukaryotic translation initiation factor 3 subunit A (EIF3A) [73] (Table 2)
T cells, reinforce cancer immunosurveillance, and improve the efficacy of mitoxantrone as well as oxaliplatin [83]. Such discrepancy could be due to the fact that cellular factors involved in the process of autophagy regulate other cellular responses, such as cytokinesis, endocytosis, cell growth, and cell death, in an autophagy-independent manner, and that the effects of autophagy on the fate of cancer cells are dependent on p53 status [84,85,86]
Summary
Cancer cells may initially respond to treatment, not all cells are eliminated. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of miRNA levels, through either the inhibition or replacement approach, has been proposed to sensitize cancer cells to other anti-cancer therapies. This combination of miRNA-based therapy with other anti-cancer therapies (hereinafter referred to as miRNA-based combinatorial cancer therapy) is attractive due to the ability of miRNAs to regulate multiple resistance-mediating pathways by targeting multiple genes. It is indispensable to experimentally investigate whether the suppression or replacement of an miRNA can enhance the efficacy of anti-cancer therapies by efficiently impeding signaling pathways associated with therapeutic resistance, since the functions of miRNAs are dependent on the type of cancer. We discuss the characteristic features of miRNAs that exert influence on the adequate efficacy of miRNA-based combinatorial cancer therapy
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