Abstract
Several lines of evidence have confirmed the magnitude of crosstalk between HGF/c-Met axis (hepatocyte growth factor and its high-affinity receptor c-mesenchymal-epithelial transition factor) and non-coding RNAs (ncRNAs) in tumorigenesis. Through activating canonical or non-canonical signaling pathways, the HGF/c-Met axis mediates a range of oncogenic processes such as cell proliferation, invasion, apoptosis, and angiogenesis and is increasingly becoming a promising target for cancer therapy. Meanwhile, ncRNAs are a cluster of functional RNA molecules that perform their biological roles at the RNA level and are essential regulators of gene expression. The expression of ncRNAs is cell/tissue/tumor-specific, which makes them excellent candidates for cancer research. Many studies have revealed that ncRNAs play a crucial role in cancer initiation and progression by regulating different downstream genes or signal transduction pathways, including HGF/c-Met axis. In this review, we discuss the regulatory association between ncRNAs and the HGF/c-Met axis by providing a comprehensive understanding of their potential mechanisms and roles in cancer development. These findings could reveal their possible clinical applications as biomarkers for therapeutic interventions.
Highlights
Cancers are initiated by genetic preconditions and epigenetic alterations, accompanied by various mechanisms, most of which are still unclear (Bach and Lee, 2018)
In vitro and in vivo studies have demonstrated that miR-101-3p inhibits Hepatocellular Carcinoma (HCC) progression by targeting Hepatocyte growth factor (HGF) and it could be regarded as another potential therapeutic tool for regulating cell proliferation and metastasis (Liu et al, 2019)
The study results showed that lncRNA GAPLINC was upregulated in Colorectal Cancer (CRC) tissues and stimulated CRC cell migration and invasion by regulating miR-34a/c-MET signal pathway (Luo et al, 2018)
Summary
Cancers are initiated by genetic preconditions and epigenetic alterations, accompanied by various mechanisms, most of which are still unclear (Bach and Lee, 2018). Studies reported that miR-200a plays an active tumor-suppressing role in non-small cell lung cancer, and could inhibit gefitinib resistance and enhance the radio-sensitivity by deactivating the HGF/c-Met pathway (Zhen et al, 2015; Du et al, 2019).
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