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Accumulating evidence suggests that long noncoding RNA (lncRNA) functions as a critical regulator in cancer biology. Here, we characterized the role of lncRNA PCED1B antisense RNA 1 (PCED1B-AS1) in glioblastoma (GBM). PCED1B-AS1 was notably upregulated in GBM tissues and cell lines and closely associated with larger tumor size and higher grade. Patients with high PCED1B-AS1 had shorter survival time than those with low PCED1B-AS1. Functional experiments showed that depletion of PCED1B-AS1 significantly inhibited, while overexpression of PCED1B-AS1 promoted cell proliferation, glucose uptake, and lactate release. Mechanistically, PCED1B-AS1 was able to directly bind to the 5′-UTR of HIF-1α mRNA and potentiate HIF-1α translation, leading to increased HIF-1α protein level, thereby promoting the Warburg effect and tumorigenesis. Importantly, PCED1B-AS1 lost the carcinogenic properties in the absence of HIF-1α. In addition, we also confirmed the existence of the PCED1B-AS1/HIF-1α regulatory axis in vivo. Taken together, our findings demonstrate that PCED1B-AS1 is a novel oncogenic lncRNA in GBM and functions in a HIF-1α-dependent manner, which provides a promising prognostic biomarker and druggable target for GBM.

LINC00473 has been reported to be aberrantly expressed in diverse kinds of human malignancy. However, the function and underlying mechanisms of LINC00473 in glioma still remain unclear. In the present study, LINC00473 was notably elevated in glioma tissues and cell lines. High LINC00473 expression was associated with advanced WHO grade (III-IV), low Karnofsky performance score (KPS), and poor prognosis. Loss function assays showed that LINC00473 knockdown decreased glioma cell proliferation, invasion and epithelial-mesenchymal transition (EMT) processes in vitro, and reduced tumor growth in vivo. Mechanistic analysis indicated that LINC00473 regulated CDK6 expression by competitively binding to miR-637. Moreover, rescue assays revealed that miR-637 inhibitors abolished the effects of LINC00473 suppression on glioma cells progression. Thus, we demonstrated that LINC00473 could act as a ceRNA of miR-637 to promote glioma progression through regulating CDK6 expression, which provided a potential therapeutic target for treatment of glioma patients.

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The concept of entropy of interval-valued intuitionistic fuzzy set (IvIFS) is Þrst introduced. The close relationships between entropy and the similarity measure of interval-valued intuitionistic fuzzy sets are discussed in detail. We also obtain some important theorems by which entropy and similarity measure of IvIFSs can be transformed into each other based on their axiomatic deÞnitions. Simultaneously, some formulae to calculate entropy and similarity measure of IvIFSs are put forward. C

We apply the turbulent convection model (TCM) to investigate properties of turbulence in the solar convective envelope, especially in overshooting regions. The results show TCM gives negative turbulent heat flux u r T in overshooting regions, which is similar to other nonlocal turbulent convection theories. The turbulent temperature fluctuation T T shows peaks in overshooting regions. Most important, we find that the downward overshooting region below the base of the solar convection zone is a thin cellular layer filled with roll-shaped convective cells. The overshooting length for the temperature gradient is much shorter than that for element mixing because turbulent heat flux of downward and upward moving convective cells counteract each other in this cellular overshooting region. Comparing the models' sound speed with observations, we find that taking the convective overshooting into account helps to improve the sound speed profile of our nonlocal solar models. Comparing differences of the p-mode oscillation frequencies with observations, we validated that increasing the diffusion parameters and decreasing the dissipation parameters of TCM make the p-mode oscillation frequencies of the solar model be in better agreement with observations.