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The miR-92a family, including miR-25, miR-92a-1, miR-92a-2 and miR-363, arises from three different paralog clusters miR-17-92, miR-106a-363, and miR-106b-25 that are highly conservative in the process of evolution, and it was thought as a group of microRNAs (miRNAs) correlated with endothelial cells. Aberrant expression of miR-92a family was detected in multiple cancers, and the disturbance of miR-92a family was related with tumorigenesis and tumor development. In this review, the progress on the relationship between miR-92a family and their target genes and malignant tumors will be summarized.

MicroRNAs (miRNAs) are a class of endogenous, non-coding, 18-24 nucleotide length single-strand RNAs that could modulate gene expression at post-transcriptional level. Previous studies have shown that miR-128 enriched in the brain plays an important role in the development of nervous system and the maintenance of normal physical functions. Aberrant expression of miR-128 has been detected in many types of human tumors and its validated target genes are involved in cancer-related biological processes such as cell proliferation, differentiation and apoptosis. In this review, we will summarize the roles of miR-128 and its target genes in tumorigenesis and metastasis.

Recently, van der Waals heterostructures (vdWHs) have trigged intensive interest due to their novel electronic and optoelectronic properties. The vdWHs could be achieved by stacking two dimensional layered materials (2DLMs) on top of another and vertically kept by van der Waals forces. Furthermore, organic semiconductors are also known to interact via van der Waals forces, which offer an alternative for the fabrication of organic-inorganic p-n vdWHs. However, the performances of organic-inorganic p-n vdWHs produced so far are rather poor, owing to the unmatched electrical property between the 2DLMs and organic polycrystalline films. To make improvements in such novel heterostructure architectures, here we adopt high quality organic single crystals instead of polycrystalline films to construct a pentacene/MoS p-n vdWH. The vdWHs show a much higher current density and better anti-ambipolar characteristics with a highest transconductance of 211 nS. Moreover, device configuration-dependent transfer characteristics are demonstrated and a mechanism of a gate bias modulated vertical space charge zone existing at the vertical p-n vdWHs interface is proposed. These findings provide a new route to optimize the organic-inorganic p-n vdWHs and a guideline for studying the intrinsic properties of vdWHs.

BackgroundAccumulating evidences indicate that circRNAs play important roles in the progression and chemoresistance of human cancers. The present study is designated for researching the roles of circ_0003418 in hepatocellular carcinoma (HCC).MethodsWe detected the expression profile of circ_0003418 in human HCC tissues and cell lines by quantitative real-time-PCR assays. CCK-8 assay, transwell migration assay, transwell invasion assay and drug-sensitivity analysis were carried out to estimate the effects of circ_0003418 on HCC cells' proliferation, migration, invasion and resistance to cisplatin, respectively. Mouse xenograft model was conducted to monitor the role of circ_0003418 in cisplatin resistance in vivo. Western blotting was performed to explore the changes of the Wnt/β-catenin pathway after knockdown of circ_0003418. The rescue experiment was carried out to explore circ_0003418-activated biological functions through Wnt/β-catenin pathway.ResultsThe expression level of circ_0003418 was downregulated in HCC tissues and cell lines, and the level correlated with tumor size, TNM stage and HBsAg level in HCC patients. circ_0003418 knockdown promoted HCC cells' proliferation, migration, and invasion. Additionally, suppression of circ_0003418 enhanced cisplatin resistance of HCC cells in vivo and vitro. Knockdown of circ_0003418 activated the Wnt/β-catenin signalling pathway in HCC cells. The effect of circ-0003418 on sensitivity of HCC cells to cisplatin was reversed after inhibition of Wnt/β-catenin pathway.Conclusioncirc-0003418 exerts an antitumorigenic role in HCC and advances the sensitivity of HCC cells to cisplatin by restraining the Wnt/β-catenin pathway. Thus, circ-0003418 may represent a novel biomarker and provide us a new strategy for the treatment of HCC.

Long non-coding RNA (lncRNA) and microRNA (miRNA) play an important role in genesis and progression of tumors. The aim of this study was to explore the expression, biological function and molecular mechanism of small nucleolar RNA host gene 16 (SNHG16) in HCC. RT-qPCR was conducted to evaluate the expression level of SNHG16 in HCC tissues and cell lines. Our findings showed for the first time that SNHG16 was up-regulated in HCC tissues and cell lines. The expression of SNHG16 in cancer tissues was highly correlated with tumor size, TNM stage, ALT expression level and HBV DNA level. Moreover, cell proliferation, migration and invasion were detected by CCK-8 assay, transwell migration assay and transwell invasion assay, respectively. Xenograft tumor experiment was used to determine the biological function of SNHG16 in vivo . As revealed by our data, SNHG16 accelerated the proliferation, migration and invasion of HCC cell. SNHG16 facilitated tumor formation in vivo . Next, the relationship between SNHG16, miR-186 and ROCK1 were analyzed using bioinformatics analysis, qRT-PCR, luciferase reporter assay and western blot. Further molecular mechanism studies reported that the expression of SNHG16 was negatively correlated with the level of miR-186 and SNHG16 directly bound to miR-186. SNHG16 and miR-186 repressed each other. Notably, rescue experiments were conducted and showed that miR-186 reversed the effect of SNHG16 on cell. Taken together, SNHG16 promoted HCC cell proliferation, migration and invasion by functioning as a competitive endogenous RNA (ceRNA) to negatively regulate miR-186 expression. Our data suggested that SNHG16 might be a potential biomarker and a new therapeutic target for HCC.

By designing a few-layer boron nitried (BN) buffer layer, topological crystalline insulator Pb(1-x)Sn(x)Se nanoplates are directly grown on SiO2/Si, which shows high compatibility with current Si-based integrated circuit technology. Back-gated field-effect transistors of Pb(1-x)Sn(x)Se nanoplates exhibit a room-temperature carrier mobility of 0.73-4.90 cm(2) V(-1) s(-1), comparable to layered materials and molecular crystals, and high-efficiency mid-IR detection (1.9-2.0 μm).

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