Diffuse large B cell lymphoma (DLBCL) is one of the most common types of malignancy worldwide. The lack of clear symptoms and early detection make it difficult to diagnose at an early stage, leading to poor prognosis of the patients. Long non-coding RNAs (lncRNAs) have come into focus for their important regulatory roles in fundamental biological processes, particularly in cancer initiation, development and progression. The aim of the present study was to investigate the expression of lncRNA Hox transcript antisense intergenic RNA (HOTAIR) in a cohort of patients with DLBCL to assess its clinical value and biological function in DLBCL. The reverse transcription-polymerase chain reaction was used to detect HOTAIR expression levels and cells were transfected with small interfering RNA to compare cell proliferation, cell cycle progression and apoptosis. Western blotting was also conducted to detect possible signaling pathways. It was first found that the expression levels of HOTAIR were upregulated in DLBCL tumor tissues and cell lines, compared with normal tissues and cells. In addition, HOTAIR was significantly correlated with tumor size, clinical stage, B symptoms and International Prognostic Index scores; and higher expression levels of HOTAIR were correlated with improved prognosis. Univariate and multivariate analyses verified that HOTAIR was a key independent predictive factor for DLBCL prognosis. Furthermore, it was revealed that the knockdown of the expression of HOTAIR led to growth inhibition, cell cycle arrest and apoptosis in vitro, possibly through the phosphoinositide 3-kinase/AKT/nuclear factor-κB pathway. These results suggested that HOTAIR may be regarded as a novel indicator of poor prognosis, and may serve as a potential target for gene therapy in the treatment of DLBCL.
Many microRNAs (miRs) have been demonstrated to play promoting or tumor suppressive roles in human cancers including breast cancer. However, the molecular mechanism of miR-133a underlying the malignant progression of breast cancer still remains obscure. In the present study we observed that the expression of miR-133a was significantly downregulated in breast cancer tissues and cell lines, when compared with adjacent non-tumor tissues and normal breast cell line, respectively. Reduced miR-133a levels were significantly associated with advanced clinical stage, lymph node metastasis, as well as shorter survival time of patients with breast cancer. Restoration of miR-133a expression led to significant decrease in the proliferation, migration, and invasion of SK-BR-3 and MDA-MB-231 cells in vitro, as well as in tumor xenograft growth in nude mice. Luciferase reporter gene assay data identified LASP1 as a target gene of miR-133a, and the expression of LASP1 was negatively regulated by miR-133a in breast cancer cells. LASP1 was significantly upregulated in breast cancer tissues and cell lines, and its upregulation was significantly associated with disease progression. siRNA-induced LASP1 downregulation caused a significant reduction in breast cancer cell proliferation, migration and invasion. Furthermore, overexpression of LASP1 impaired the suppressive effects of miR-133a upregulation on the proliferation, migration and invasion of SK-BR-3 and MDA-MB-231 cells. In summary, the present study demonstrates that miR-133a acts as a tumor suppressor in breast cancer partly at least via targeting LASP1, and thus suggests that the miR-133a/LASP1 axis may become a potential therapeutic target for breast cancer.
Algorithms for mobile robotic systems are generally implemented on purely digital computing platforms. Developing alternative computational platforms may lead to more energy-efficient and responsive mobile robotics. Here, we report a hybrid analog-digital computing platform enabled by memristors on a mobile inverted pendulum robot. Our mobile robotic system can tune the conductance states of memristors adaptively using a model-free optimization method to achieve optimal control performance. We implement sensor fusion and the motion control algorithms on our hybrid analog-digital computing platform and demonstrate more than one order of magnitude enhancement of speed and energy efficiency over traditional digital platforms.
Plasmon-enhanced fluorescence is demonstrated in the vicinity of metal surfaces due to strong local field enhancement. Meanwhile, fluorescence quenching is observed as the spacing between fluorophore molecules and the adjacent metal is reduced below a threshold of a few nanometers. Here, we introduce a technology, placing the fluorophore molecules in plasmonic hotspots between pairs of collapsible nanofingers with tunable gap sizes at sub-nanometer precision. Optimal gap sizes with maximum plasmon enhanced fluorescence are experimentally identified for different dielectric spacer materials. The ultrastrong local field enhancement enables simultaneous detection and characterization of sharp Raman fingerprints in the fluorescence spectra. This platform thus enables in situ monitoring of competing excitation enhancement and emission quenching processes. We systematically investigate the mechanisms behind fluorescence quenching. A quantum mechanical model is developed which explains the experimental data and will guide the future design of plasmon enhanced spectroscopy applications.
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