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MYB transcription factors (TFs), as one of the largest gene families in plants, play important roles in multiple biological processes, such as plant growth and development, cell morphology and pattern building, physiological activity metabolism, primary and secondary metabolic reactions, and responses to environmental stresses. The function of MYB TFs in crops has been widely studied, but few studies have been done on medicinal plants. In this review, we summarized the MYB TFs that play important roles in secondary metabolism and emphasized the possible mechanisms underlying how MYB TFs are regulated at the protein, posttranscriptional, and transcriptional levels, as well as how they regulate the downstream target gene networks related to secondary metabolism in plants, especially in medicinal plants.

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Background and Aims Long noncoding RNAs (lncRNAs) have been associated with infection and hepatitis B virus (HBV)‐related diseases, though the underlying mechanisms remain unclear. Approach and Results We obtained HBV‐HCC lncRNA profiles by deep sequencing and found HOXA distal transcript antisense RNA (HOTTIP) to be significantly up‐regulated. RT‐qPCR indicated that HOTTIP is highly expressed in HBV‐positive hepatoma tissue and induced by HBV in vitro. Virological experiments showed that HOTTIP significantly suppresses the generation of hepatitis B viral surface antigen, hepatitis B viral e antigen and HBV replication. Homeobox A13 (HOXA13), a downstream factor of HOTTIP, was found to bind to HBV enhancer I and X promotor to repress the production of HBV pregenome RNA (pgRNA) and total RNA as well as HBV replication, suggesting that HOXA13 mediates HOTTIP‐induced suppression of HBV replication. More interestingly, HBV DNA polymerase (DNA pol) binds to and stabilizes cAMP‐responsive element‐binding protein 1 (CREB1) mRNA to facilitate translation of the protein, which, in turn, binds to the regulatory element of HOTTIP to promote its expression. Conclusions Our findings demonstrate that HBV DNA pol attenuates HBV replication through activation of the CREB1‐HOTTIP‐HOXA13 axis. These findings shed light on the mechanism by which HBV restrains replication to contribute to persistent infection.

Long non-coding RNAs (lncRNAs) have been reported to be involved in the development and progression of hepatocellular carcinoma (HCC). However, few studies have focus on the dyregulation and the role of lncRNAs in HBV-related HCC. We performed a comprehensive analysis of lncRNAs expression profile in HBV-related HCC tissues samples using deep sequencing. We revealed that a total of 1242 lncRNA transcripts (983 up-regulated and 259 down-regulated) and 1841 mRNA transcripts were significantly differentially expressed in HBV-related HCC patients. Pathway and gene ontology analysis showed that they are involved in the biological process related to HCC development by cis-regulation of co-expressed protein-coding genes. 10 candidate lncRNAs were selected and validated with quantitative real-time PCR analysis. Furthermore, we found that one of most down-regulated lncRNAs, n346077, could suppress HCC cells invasion and migration in vitro. Our findings provide an overview of aberrantly expressed lncRNAs in HBV-related HCC and will be useful for further functional studies of lncRNAs in HBV-related pathogenesis.