Background: Increased long noncoding RNA (lncRNA) expression is characteristic to hepatocellular carcinoma (HCC) and several other neoplasms. The present study aimed to identify the mechanism underlying modulation of HCC development by the lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). Methods: Quantitative real-time polymerase chain reaction was used to determine MALAT1 and microRNA (miR)-146a expression in HCC tissues and cell lines. Western blotting was performed to measure PI3K, Akt, and mTOR levels. Dual-luciferase reporter assay was used to validate the direct targeting and negative regulatory interaction between miR-146a and MALAT1. Cell viability, proliferation, and apoptosis were analyzed using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, colony formation assay, and flow cytometry, respectively; autophagy was detected based on LC3B expression. Results: MALAT1 expression was higher in HCC tissues than in normal tissues. MALAT1 upregulation promoted HCC cell proliferation, whereas MALAT1 downregulation promoted HCC apoptosis and autophagy. Moreover, effects of MALAT1 downregulation on HCC cells were abolished by miR-146a inhibition. miR-146a directly targeted the 3′-untranslated region of PI3K, and PI3K protein level was clearly decreased upon miR-146a mimic transfection. Conclusions: MALAT1 may modulate HCC cell proliferation, apoptosis, and autophagy via sponging miR-146a, which regulates HCC progression.

Dysregulation of genes involved in alternative splicing contributes to hepatocarcinogenesis. SNRPB, a component of spliceosome, is implicated in human cancers, yet its clinical significance and biological function in hepatocellular carcinoma (HCC) remains unknown. Here, we show that SNRPB expression is increased in HCC tissues, compared with the nontumorous tissues, at both messenger RNA and protein levels in two independent cohorts. High expression of SNRPB is significantly associated with higher pathological grade, vascular invasion, serum alpha-fetoprotein level, tumor metastasis, and poor disease-free and overall survivals. Luciferase reporter and chromatin immunoprecipitation assays demonstrate that SNRPB upregulation in HCC is mediated by c-Myc. Positive correlation is found between SNRPB and c-Myc expression in clinical samples. In vitro studies show that ectopic expression of SNRPB promotes HCC cell proliferation and migration, whereas knockdown of SNRPB results in the opposite phenotypes. Collectively, our data suggest SNRPB function as an oncogene and serve as a potential prognostic factor in HCC.

Lead-free piezoelectric material-based ultrasonic transducers have been researched for several years, but the inefficient properties and design difficulties have troubled lead-free ultrasonic transducers for a long time. To improve the performance and design efficiency of lead-free ultrasonic transducers, in this work, an equivalent circuit model and intelligent optimization algorithm were combined for use in a transducer design. Firstly, 0.94(Bi0.5Na0.5)TiO3-0.06BaTiO3(BNT-6BT) lead-free piezoelectric ceramics were prepared and characterized. Then, BNT-6BT ceramics were used to fabricate the ultrasonic transducers. An equivalent circuit model-based software, PiezoCAD, and a genetic algorithm-based back-propagation neural network were used to optimize the design of the transducers. A 3.03 MHz center frequency and 60.3% −6 dB bandwidth of the optimized transducers were achieved, which were consistent with the neural networks optimization results. To verify the application potential of the lead-free transducers, tungsten rods phantom imaging and polystyrene spheres with 300 μm diameter manipulation were completed by the transducers, and the experiment results indicate that the BNT-6BT lead-free transducers have great potential in further biological and biomedical applications.