BackgroundAs a major component of plant cell wall, lignin plays important roles in mechanical support, water transport, and stress responses. As the main cause for the recalcitrance of plant cell wall, lignin modification has been a major task for bioenergy feedstock improvement. The study of the evolution and function of lignin biosynthesis genes thus has two-fold implications. First, the lignin biosynthesis pathway provides an excellent model to study the coordinative evolution of a biochemical pathway in plants. Second, understanding the function and evolution of lignin biosynthesis genes will guide us to develop better strategies for bioenergy feedstock improvement.ResultsWe analyzed lignin biosynthesis genes from fourteen plant species and one symbiotic fungal species. Comprehensive comparative genome analysis was carried out to study the distribution, relatedness, and family expansion of the lignin biosynthesis genes across the plant kingdom. In addition, we also analyzed the comparative synteny map between rice and sorghum to study the evolution of lignin biosynthesis genes within the Poaceae family and the chromosome evolution between the two species. Comprehensive lignin biosynthesis gene expression analysis was performed in rice, poplar and Arabidopsis. The representative data from rice indicates that different fates of gene duplications exist for lignin biosynthesis genes. In addition, we also carried out the biomass composition analysis of nine Arabidopsis mutants with both MBMS analysis and traditional wet chemistry methods. The results were analyzed together with the genomics analysis.ConclusionThe research revealed that, among the species analyzed, the complete lignin biosynthesis pathway first appeared in moss; the pathway is absent in green algae. The expansion of lignin biosynthesis gene families correlates with substrate diversity. In addition, we found that the expansion of the gene families mostly occurred after the divergence of monocots and dicots, with the exception of the C4H gene family. Gene expression analysis revealed different fates of gene duplications, largely confirming plants are tolerant to gene dosage effects. The rapid expansion of lignin biosynthesis genes indicated that the translation of transgenic lignin modification strategies from model species to bioenergy feedstock might only be successful between the closely relevant species within the same family.

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The evolution of glyphosate resistance in weedy species places an environmentally benign herbicide in peril. The first report of a dicot plant with evolved glyphosate resistance was horseweed, which occurred in 2001. Since then, several species have evolved glyphosate resistance and genomic information about nontarget resistance mechanisms in any of them ranges from none to little. Here, we report a study combining iGentifier transcriptome analysis, cDNA sequencing, and a heterologous microarray analysis to explore potential molecular and transcriptomic mechanisms of nontarget glyphosate resistance of horseweed. The results indicate that similar molecular mechanisms might exist for nontarget herbicide resistance across multiple resistant plants from different locations, even though resistance among these resistant plants likely evolved independently and available evidence suggests resistance has evolved at least four separate times. In addition, both the microarray and sequence analyses identified non–target-site resistance candidate genes for follow-on functional genomics analysis.

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Hepatocellular carcinoma (HCC) causes high morbidity and mortality due to a lack of adequate treatments. Cancer treatments have benefited from nanotechnology approaches that integrate multimodal synergistic therapies. A synergistic, minimally invasive strategy of interventional photo dynamic therapy (IPDT) and chemotherapy for HCC treatment through percutaneous transperitoneal puncture is disclosed that is based on photosensitive porphyrinic galactose-modified metal-organic frameworks (PCN-224) first used as hepatic targeting and encapsulated with anticancer drug doxorubicin (DOX@Gal-PCN-224). Real-time imaging reveals the effective accumulation of the integrated nanosystem in the HCC cells and tumor tissues due to hepatic targeting. Evaluation of the anti-tumor efficiency of this nanosystem on orthotopic transplantation tumors with the aid of minimally invasive intervention shows a tumor inhibition rate of 98%. The synergistic effects induce high-level cell apoptosis and tissue necrosis in vitro and in vivo. This bimodal IPDT/chemotherapy strategy holds great potential in the clinical treatment for HCC.

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As one of the most common and aggressive cancer types, hepatocellular carcinoma (HCC) leads to a large number of fatalities every year. However, the pathogenesis of HCC remains largely unknown. In the present study, it was identified that FEZF1-AS1 was significantly upregulated in HCC cell lines and tissues, as determined by reverse transcription-quantitative polymerase chain reaction. Additionally, it was observed that higher expression of FEZF1-AS1 in patients with HCC indicated poorer prognosis. Furthermore, it was identified that knockdown of FEZF1-AS1 markedly inhibited the proliferation, colony formation, migration and invasion of Hep3B and Huh7 cells, as determined by Cell Counting Kit-8, colony formation and Transwell assays. In terms of mechanism, it was observed that FEZF1-AS1 acted as a sponge for microRNA (miR)-4443. The results of a luciferase reporter assay revealed that overexpression of miR-4443 significantly inhibited the luciferase activity in Hep3B and Huh7 cells. Additionally, miR-4443 overexpression markedly inhibited the expression of FEZF1-AS1, and vice versa. It was additionally identified that miR-4443 was downregulated in HCC tissues. There was an inverse correlation between the expression of miR-4443 and FEZF1-AS1 in HCC tissues. Furthermore, through functional experiments, it was identified that knockdown of FEZF1-AS1 significantly inhibited the proliferation, migration and invasion of HCC cells, whereas inhibition of miR-4443 reversed these effects. Collectively, the present results demonstrated that FEZF1-AS1 acts as an oncogene by acting as a sponge for miR-4443.

Tert-butylhydroquinone (tBHQ), an inducer of nuclear factor erythroid 2-related factor 2 (Nrf2), has been demonstrated to attenuate oxidative stress-induced injury and the apoptosis of human neural stem cells and other cell types. However, whether tBHQ is able to exert a protective effect against oxidative stress and the apoptosis of cardiomyocytes has not yet been determined. Thus, the objective of the present study was to determine whether tBHQ protects H9c2 cardiomyocytes against ethanol-induced apoptosis. For this purpose, four sets of experiments were performed under standard culture conditions as follows: i) untreated control cells; ii) cell treatment with 200 mM ethanol; iii) cell treatment with 5 µM tBHQ; and iv) cell pre-treatment with 5 µM tBHQ for 24 h, followed by medium change and co-culture with 200 mM ethanol containing 5 µM tBHQ for a further 24 h. The viability of the cardiomyocytes was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of intracellular reactive oxygen species (ROS) and apoptosis were assessed by flow cytometry. Protein expression was measured by western blot analysis, and Nrf2 nuclear localization was observed by immunofluorescence. Exposure to ethanol led to a decrease in the protein expression of Nrf2 and its downstream antioxidant enzymes, accompanied by an increase in ROS generation and in the apoptosis of H9c2 cells. Pre-treatment with tBHQ significantly prevented the H9c2 cells from undergoing ethanol-induced apoptosis. tBHQ also increased the expression of B-cell lymphoma-2 (Bcl-2), whereas Bcl-2-associated X protein (Bax) expression was decreased. tBHQ promoted Nrf2 nuclear localization and increased the expression of Nrf2, superoxide dismutase (SOD), catalase (CAT) and heme oxygenase-1 (HO-1), and simultaneously inhibited the ethanol-induced overproduction of intracellular ROS. Therefore, tBHQ confers protection against the ethanol-induced apoptosis of and activates the Nrf2 antioxidant pathway in H9c2 cardiomyocytes.