Abstract
Gastric cancer is the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide. Advanced gastric cancer patients can notably benefit from chemotherapy including adriamycin, platinum drugs, 5-fluorouracil, vincristine, and paclitaxel as well as targeted therapy drugs. Nevertheless, primary drug resistance or acquisition drug resistance eventually lead to treatment failure and poor outcomes of the gastric cancer patients. The detailed mechanisms involved in gastric cancer drug resistance have been revealed. Interestingly, different noncoding RNAs (ncRNAs), such as microRNAs (miRNAs), long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs), are critically involved in gastric cancer development. Multiple lines of evidences demonstrated that ncRNAs play a vital role in gastric cancer resistance to chemotherapy reagents and targeted therapy drugs. In this review, we systematically summarized the emerging role and detailed molecular mechanisms of ncRNAs impact drug resistance of gastric cancer. Additionally, we propose the potential clinical implications of ncRNAs as novel therapeutic targets and prognostic biomarkers for gastric cancer.
Highlights
Gastric cancer is a malignant tumor originating from the gastric mucosa
The development of multi-drug resistance (MDR) of gastric cancer cells is a major hurdle in clinical oncology, which may result in a poor prognosis
The complicated mechanisms involved in gastric cancer MDR include inactivation of apoptosis signaling pathways, loss of cell cycle checkpoint control, accelerated cell proliferation and autophagy flux, enhanced DNA damage repair capacity, diminished uptake and/or increased efflux of drugs via upregulated MDR-associated proteins, activated cancer stem cells (CSCs), as well as epithelialmesenchymal transition (EMT) [2,3,4]
Summary
Gastric cancer is a malignant tumor originating from the gastric mucosa. As the fourth most common malignancy and the third leading cause of cancer-related deaths worldwide, there were about 984,000 new gastric cancer cases and 841,000 deaths occurred in 2013 [1]. Exogenous expression of miR-106a enhanced the resistance to DDP of gastric cancer cells by inhibiting the PTEN/Akt signaling pathway and tumor suppressive RUNX3 [84, 85]. MiR-421, a highly expressed miRNA in advanced gastric cancer patients, could promote gastric cancer metastasis and DDP resistance through inhibiting E-cadherin and caspase-3 expression, in vivo and in vitro [91].
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