Abstract
Primary liver cancer [hepatocellular carcinoma (HCC)] is one of the most common malignant tumors worldwide, causing serious health threats because of its high morbidity and mortality, rapid growth, and strong invasiveness. Patients with HCC frequently develop resistance to the current chemotherapeutic drugs, and this is largely attributed to the high-level heterogeneity of the tumor tissue. MicroRNAs (miRNAs) are a group of master regulators for multiple physiological and pathological processes and play important roles in the tumorigenesis. More recent studies have indicated that miRNAs also play a non-negligible role in the development of drug resistance in liver cancer. In this review, we summarize the data from the latest studies on the mechanisms of drug resistance in liver cancer, including autophagy, membrane transporters, epithelial–mesenchymal transitions (EMTs), tumor microenvironment, and genes and proteins that are associated with apoptosis. The data herein will provide valuable information for the development of novel approaches to tackle drug resistance in the management of liver cancer.
Highlights
Primary liver cancer is one of the most common malignant tumors in the worldwide and is a serious health threat to humans because of its high morbidity and mortality, rapid growth, and strong invasiveness [1]
Surgical resection is the first choice for the treatment of early primary liver cancer, but this treatment approach carries high recurrence rate and high rate of postsurgery metastasis, because most hepatocellular carcinoma (HCC) patients are generally diagnosed at the advanced stage, and only palliative treatments such as chemotherapy can be used for treatment
In Histone deacetylase inhibitors (HDACis)-induced autophagy, nuclear factor erythroid 2 like-2 (Nrf2) positively regulates mTOR through miR-129-3p, and HDACi-mediated cell death can be enhanced by inhibiting miRNA-129-3p [28]
Summary
Primary liver cancer is one of the most common malignant tumors in the worldwide and is a serious health threat to humans because of its high morbidity and mortality, rapid growth, and strong invasiveness [1]. In HDACi-induced autophagy, Nrf2 positively regulates mTOR through miR-129-3p, and HDACi-mediated cell death can be enhanced by inhibiting miRNA-129-3p [28]. Yuan et al [30] have found that the mechanism may be related to autophagy caused by a high expression of LC3-II and downregulation of p62 in drug-resistant cells, and MALAT1-miR-216b axis modulates MDR of HCC cells by participating in the regulation of autophagy.
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