The Heptazine-Based Materials through Intrinsically Modification for the Cycloaddition of CO2 and Bisepoxides.

For the efficient utilization of CO2 into valuable product, the attractive carbon nitride catalysts have been widely studied. In this work, heptazine-related materials with varying degree of polymerization were designed by an intrinsically modification strategy and employed in the cycloaddition of CO2 with the bisepoxide 1, 4-butanediol diglycidyl ether (BDODGE). We initially figured out that the sample prepared at 450 °C contained more melem hydrate, exhibiting the best performance. The epoxides conversion and corresponding cyclic carbonates selectivity could achieve 93.1 % and 99.3 % at 140 °C for 20 h without any cocatalyst and solvent, respectively. Results of the catalytic tests suggested that the high catalytic activity was dependent on big size porous structure and the synergetic effect of active amino groups and -OH groups. The role of water in maintaining the specific structure and providing active site has been proved. Moreover, the CN-450-W catalyst exhibited outstanding recycling stability. And finally, a plausible reaction mechanism was proposed.

Location deviation compensation based on maximum cross correlation in optical frequency domain reflectometry.

A location deviation compensation algorithm based on maximum cross correlation is proposed for optical frequency domain reflectometry. The characteristic change of fiber under test and the auxiliary interferometer induced by strain/temperature causes location deviation in the optical frequency domain reflectometry system, which in turn leads to demodulation errors. Compared to current available compensated methods, this algorithm simultaneously compensates the location deviation caused by the fiber under test and the auxiliary interferometer. The temperature variation experiments of the fiber under test and the auxiliary interferometer were carried out, respectively, and results show that the algorithm minimized the demodulation errors introduced by the location deviation.

circRNA_103615 contributes to tumor progression and cisplatin resistance in NSCLC by regulating ABCB1.

Lung cancer is one of the main causes of tumor lethality worldwide. Circular RNAs (circRNAs) have essential roles in tumor progression. However, in non-small cell lung carcinoma (NSCLC), the role of circRNAs remains unknown. In the present study, the expression, function and molecular mechanisms of a new circRNA, circRNA_103615, were investigated in NSCLC. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect circRNA_103615 expression levels in NSCLC and normal tissues, as well as in NSCLC cell lines. MTT assay, flow cytometric assay, colony formation assay, and cell migration and invasion assays were used to examine the function of circRNA_103615 in NSCLC cells. MTT assay, colony formation assay, RT-qPCR, and western blotting were used to detect the effect of circRNA_103615 on cisplatin resistance. The results demonstrated that NSCLC cell lines and tissues had increased levels of circRNA_103615 compared with normal cells and normal tissues, respectively. Functionally, silencing of circRNA_103615 by small interfering RNA resulted in suppression of cell growth, migration, and invasion, but promotion of cell apoptosis. In addition, the cisplatin resistance of NSCLC was reversed by the silencing of circRNA_103615. Notably, ATP binding cassette subfamily Bmember 1 (ABCB1) expression was significantly decreased following circRNA_103615 knockdown, and ABCB1 overexpression reversed the effects of circRNA_103615 silencing on NSCLC cisplatin resistance. Thus, the present study indicated that circRNA_103615 may serve as a critical oncogene and potential novel biomarker in NSCLC, as well as a potential cisplatin resistance promoter, by regulating ABCB1 expression.

ARRB2 promotes colorectal cancer growth through triggering WTAP.

Colorectal cancer (CRC) is one of the most lethal cancers worldwide. The expression of ß-arrestin2 (ß-Arr2, ARRB2) in CRC has been well investigated; however, its exact mechanism causing the cancer progression remains unclear. In this study, we discovered that the expression level of ARRB2 was significantly upregulated in CRC as compared to the normal tissues by employing the Cancer Genome Atlas (TCGA) data, western blot analysis, and immunohistochemistry. Furthermore, the level of ARRB2 was correlated with the patients' overall survival by Kaplan-Meier analysis. The higher expression of ARRB2 promoted CRC cell growth, enhanced the cell motility, and blocked cell apoptosis, which is crucial for tumor growth. Lastly, the suppression of ARRB2 expression was enough to attenuate the progression of CRC induced by azoxymethane/dextran sodium sulfate. Interestingly, we also found that the knockdown of ARRB2 decreased several cancer pathways mediated by the expression of Wilms tumor 1 associated protein (WTAP), which led to the inhibition of cell proliferation and migration. Altogether, our results demonstrated that ARRB2 promoted the growth and migration of CRC cells by regulating the WTAP expression.

Overexpression of MiR-146a-5p Upregulates lncRNA HOTAIR in Triple-Negative Breast Cancer Cells and Predicts Poor Prognosis.

MiR-146a-5p plays different roles in different types of cancers. We showed that miR-146a-5p and long noncoding RNA HOTAIR were both upregulated in triple-negative breast cancer. Follow-up study showed that high levels of miR-146a-5p and HOTAIR in tumor tissues were closely correlated with poor survival. MiR-146a-5p and HOTAIR were positively correlated in tumor tissues. MiR-146a-5p positively regulated HOTAIR triple-negative breast cancer cells, while HOTAIR showed no regulatory effects on miR-146a-5p expression. MiR-146a-5p and HOTAIR positively regulated the migration and invasion of triple-negative breast cancer cells. In addition, HOTAIR silencing attenuated the effects of miR-146a-5p. Therefore, overexpression of miR-146a-5p may promote triple-negative breast cancer cell invasion and migration by upregulating HOTAIR.