Abstract
Tumor metastasis is the main cause of death in patients with solid tumors. The epithelial-mesenchymal transition (EMT) process, in which epithelial cells are converted into mesenchymal cells, is frequently activated during cancer invasion and metastasis. MicroRNAs (miRNAs) are small, non-coding RNAs that provide widespread expressional control by repressing mRNA translation and inducing mRNA degradation. The fundamental roles of miRNAs in tumor growth and metastasis have been increasingly well recognized. A growing number of miRNAs are reported to regulate tumor invasion/metastasis through EMT-related and/or non-EMT–related mechanisms. In this review, we discuss the functional role and molecular mechanism of miRNAs in regulating cancer metastasis and EMT.
Highlights
Tumor metastasis is the main cause of death in patients with solid tumors
epithelial-mesenchymal transition (EMT) is regulated by a variety of signaling pathways that originate from the tumor stroma, including transforming growth factor-β (TGF-β), hepatocyte growth factor (HGF), and epidermal growth factor (EGF)[4]
A hallmark of EMT is the loss of E-cadherin (CDH1), a transmembrane glycoprotein that forms the core of adheren junctions between adjacent epithelial cells and plays a critical role in cell-to-cell adhesion[5,6]
Summary
ZEB1/2, SNAI1/2, P53 ZEB1, SNAI1/2 NA TGF-β SNAI1, P53 SNAI2 NA NA NA NA MYC NA FOSL1 SMAD4 TGF-β NA NA NA NA. Regulation of Cancer Metastasis by Pro-EMT miRNAs miR-200 family members and miR-203 are biomarkers of the epithelial and differentiated phenotype and are considered inducers of MET. MiR-9 directly targets CDH1, leading to increased cell invasiveness and a context-dependent EMT-like conversion[36]. Increased miR-92a expression reduces CDH1 expression, resulting in the promotion of cancer cell motility and invasiveness . MiR-221/222, identified as a cluster of basal-like, subtypespecific miRNAs, promote EMT in breast cancer cells by targeting trichorhinophalangeal 1 (TRPS1)–mediated inhibition of ZEB2[39]. [41] In addition, miR-216a/217 induced EMT and promoted drug resistance and recurrence by targeting PTEN and SMAD7 in liver cancer[42]. Cancer cells exploit these miRNAs to regulate the EMT/MET-associated cancer metastasis by targeting different genes involved in EMT/MET process
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