Garner Duncan (sheeplight16)

While overexpressing MICAL-L2 increased NSCLC cell proliferation, MICAL-L2 depletion decreased the proliferation of NSCLC cells, an effect that was linked to cell cycle arrest. MICAL-L2 physically interacted with the c-Myc protein and functioned to maintain nuclear c-Myc levels and prolonged its half-life. Knockdown of MICAL-L2 expression led to decreased c-Myc protein stability through accelerating polyubiquitylation of c-Myc and gave rise to c-Myc degradation. We further found that MICAL-L2 deubiquitinated c-Myc and blocked its degradation, presumably by inhibiting c-Myc phosphorylation at threonine residue 58. Conclusions These results indicate that MICAL-L2 is a key regulator of c-Myc deubiquitination and stability in the nucleus, and this activity may be involved in promoting NSCLC cell proliferation.Hepatocellular carcinoma (HCC) represents a malignant tumor predominantly arising in the setting of cirrhosis and is the third most common cause of cancer-associated death on a global scale. The heterogeneous nature of HCC and limited well-recognized biomarkers may contribute to poor patient prognosis and treatment failure. In this study, we identified expression pattern of microRNA-202-3p (miR-202-3p) in HCC and characterized its functional role as well as related mechanisms. First, we collected 50 HCC tissues and 38 normal liver tissues, and after bioinformatics prediction, the expression of miR-202-3p and KDM3A was determined in the tissues. We found lowly expressed miR-202-3p and overexpressed KDM3A in HCC tissues. Then, dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3'UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3. It has been confirmed that miR-202-3p negatively regulated KDM3A responsible for increasing the expression of HOXA1 by eliminating the histone H3 lysine 9 (H3K9)me2 in HCC cells. HOXA1 could evidently increase H3K4me1 and H3K27ac enrichment in the MEIS3 enhancer region and enhance the expression of MEIS3. Functional assays were also performed with the results showing that upregulated miR-202-3p or downregulated KDM3A retarded HCC cell viability, migration, and invasion. In addition, HepG2 cells were xenografted into nude mice, and we demonstrated that upregulated miR-202-3p reduced the growth of human HCC cells in vivo. Taken together, the present study elicits a novel miR-202-3p/KDM3A/HOXA1/MEIS3 pathway in HCC, potentiating an exquisite therapeutic target for HCC.Polyhydroxyalkanoate (PHA) bioplastic was synthesized by Burkholderia glumae MA13 from carbon sources and industrial byproducts related to sugarcane biorefineries sucrose, xylose, molasses, vinasse, bagasse hydrolysate, yeast extract, yeast autolysate, and inactivated dry yeast besides different inorganic nitrogen sources. Sugarcane molasses free of pre-treatment was the best carbon source, even compared to pure sucrose, with intracellular polymer accumulation values of 41.1-46.6% cell dry weight. Whereas, xylose and bagasse hydrolysate were poor inducers of microbial growth and polymer synthesis, the addition of 25% (v/v) sugarcane vinasse to the culture media containing molasses was not deleterious and resulted in a statistically similar maximum polymer content of 44.8% and a maximum PHA yield of 0.18 g/g, at 34°C and initial pH of 6.5, which is economic and ecologically interesting to save water required for the industrial processes and especially to offer a fermentative recycling for this final byproduct from bioethanol industry, as an alternative to its inappropriate disposal in water bodies and soil contamination. Ammonium sulfate was better even than tested organic nitrogen sources to trigger the PHA synthesis with polymer content ranging from 29.7 to 44.8%. GC-MS analysis showed a biopolymer constituted mainly of poly(3-hydroxybutyrate) although low fractions of 3-hydroxyvalerate monomer were achieved, which were n