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It has been proven that NEAT1 as a long non-coding RNA (lncRNA) is highly expressed in bladder cancer (BC). Nevertheless, the oncogenic roles of NEAT1 in BC remain largely unknown. In the present study, we observed that the RNA level of NEAT1.1, one RNA variant of NEAT1, was reduced in cisplatin-sensitive T24 cells compared to cisplatin-resistant T24 (T24R) cells after both treated with cisplatin modulated through Wnt/β-catenin signaling pathway using RNA-seq. Furthermore, NEAT1.1 was knocked down within T24R cells and caused a phenotype of the compromised cell growth, invasion and enhanced apoptosis upon cisplatin treatment compared to untreated T24R cells. Finally, c-MYC, OCT4 and p53 were determined to contribute to the transcriptional regulation of NEAT1.1 under cisplatin using ChIP assay. Taken together, our results suggest that NEAT1.1 blocking can promote the effect of cisplatin for BC treatment.

Two novel phosphrous–nitrogen-containing flame retardants (3) and (4) were successfully synthesized from two steps: condensation reaction between 4-aminopenol and 1,4-phthaladehyde (or 4,4′-biphenyldicarboxaldehyde) and addition reaction between the above condensation compounds and 9,10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide. The structures of (3) and (4) were characterized by Fourier transform infrared, nuclear magnetic resonance, and mass spectroscopy methods. The results show that (3) and (4) can serve as co-curing agents of diaminodiphenylmethane (DDM) for the curing reaction of epoxy resin. The epoxy thermosets-containing DDM and (3) or (4) exhibit moderate changes in glass transition temperature, thermal stability, and show improvement in flame retardancy: UL94 V-0 grade can be obtained when phosphorus content of the epoxy thermoset is only 1.0%; the limiting oxygen index of epoxy resin system containing (4) reaches 40.9 when phosphorus content is up to 1.5%.