Abstract
Gastric cancer (GC) is one of the most common malignant tumors of digestive systems worldwide, with high recurrence and mortality. Chemotherapy is still the standard treatment option for GC and can effectively improve the survival and life quality of GC patients. However, with the emergence of drug resistance, the clinical application of chemotherapeutic agents has been seriously restricted in GC patients. Although the mechanisms of drug resistance have been broadly investigated, they are still largely unknown. MicroRNAs (miRNAs) are a large group of small non-coding RNAs (ncRNAs) widely involved in the occurrence and progression of many cancer types, including GC. An increasing amount of evidence suggests that miRNAs may play crucial roles in the development of drug resistance by regulating some drug resistance-related proteins as well as gene expression. Some also exhibit great potential as novel biomarkers for predicting drug response to chemotherapy and therapeutic targets for GC patients. In this review, we systematically summarize recent advances in miRNAs and focus on their molecular mechanisms in the development of drug resistance in GC progression. We also highlight the potential of drug resistance-related miRNAs as biomarkers and therapeutic targets for GC patients.
Highlights
Gastric cancer (GC) is one of the most common malignant diseases of the digestive tract and the third leading cause of cancer-related deaths worldwide [1]
Most have been shown to be involved in the regulation of GC sensitivity or resistance to chemotherapeutic agents by influencing various aspect of GC cell function, including drug efflux, apoptosis, autophagy, EMT, CSCs, and cell cycle
It is easier to design specific drugs targeting them or deliver them to target tissues. These features strongly suggest that miRNAs are ideal therapeutic targets for GC patients
Summary
Gastric cancer (GC) is one of the most common malignant diseases of the digestive tract and the third leading cause of cancer-related deaths worldwide [1]. High levels of exosomal miR-21 derived from M2 macrophages have been demonstrated to facilitate CDDP resistance in GC cells by enhancing the activation of the PI3K/AKT signaling pathway via the downregulation of PTEN [74]. MiR-362 and miR-20a have been reported to activate the NF-kB signaling pathway and upregulate the expression of NF-kB-regulated genes by targeting CYLD, leading to the enhancement of the CDDP resistance of GC cells [131, 132].
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