Flavonoids are an important class of secondary metabolites widely found in plants, contributing to plant growth and development and having prominent applications in food and medicine. The biosynthesis of flavonoids has long been the focus of intense research in plant biology. Flavonoids are derived from the phenylpropanoid metabolic pathway, and have a basic structure that comprises a C15 benzene ring structure of C6-C3-C6. Over recent decades, a considerable number of studies have been directed at elucidating the mechanisms involved in flavonoid biosynthesis in plants. In this review, we systematically summarize the flavonoid biosynthetic pathway. We further assemble an exhaustive map of flavonoid biosynthesis in plants comprising eight branches (stilbene, aurone, flavone, isoflavone, flavonol, phlobaphene, proanthocyanidin, and anthocyanin biosynthesis) and four important intermediate metabolites (chalcone, flavanone, dihydroflavonol, and leucoanthocyanidin). This review affords a comprehensive overview of the current knowledge regarding flavonoid biosynthesis, and provides the theoretical basis for further elucidating the pathways involved in the biosynthesis of flavonoids, which will aid in better understanding their functions and potential uses.

Long non-coding RNAs (lncRNAs) have recently been demonstrated to serve crucial roles in various diseases including tumor initiation and progression. However, the role of the lncRNA MIR31HG in non-small cell lung cancer (NSCLC) was not well established. The present study demonstrated that MIR31HG was significantly increased in tumor tissues compared with adjacent normal tissues, and increased MIR31HG expression levels were associated with histological differentiation grade, lymph node metastasis and Tumor-node metastasis (TNM) stage in patients with NSCLC. Patients who had a higher MIR31HG expression level, were predicted a shorter over survival (OS) time. Using in vitro assays, the present study demonstrated that the downregulation of MIR31HG expression significantly inhibited cell proliferation and cell invasion abilities. Furthermore, it was identified that knockdown of MIR31HG expression suppressed the cell epithelial-mesenchymal transition (EMT) phenotype by reducing the expression levels of Twist1 and Vimentin, but also increased the expression level of E-cadherin in NSCLC cells. Furthermore, the results of the present study demonstrated that downregulated MIR31HG inhibited the Wnt/β-catenin signaling pathway by decreasing the expression of glycogen synthase kinase 3β (GSK3β) and β-catenin, but increasing the phosphorylated (p)-GSK3β expression in NSCLC cells. Together, these data demonstrated that MIR31HG could be identified as a poor prognostic biomarker and a novel therapeutic target for patients with NSCLC.

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