It is of great significance to sensitively and conveniently detect trace UO 2 2+ ions in biological and environmental samples due to severe health risks. However, such suitable sensors are still scarce. In this work, DNAzyme-based hydrogels modified on Ag NP-grafted PAN nanorods array as flexible SERS biosensor have been developed for ultrasensitive UO 2 2+ ion detection. They were first formed by the substrate strand and enzyme strand comprising the main cleavage-reaction stem-loop complex. Then, a UO 2 2+ ions responsive smart hydrogel capsule was achieved by DNAzyme complex hybridized with DNA polyacrylamide chains. Raman reporter RhB was introduced and intentionally trapped inside the hydrogel. In the absence of UO 2 2+ ions, a tiny Raman signal was presented because RhB was trapped inside the hydrogel and far away from SERS substrates. Conversely, the responsive hydrogel could be specifically attacked by UO 2 2+ ions to release RhB, leading to a strong Raman signal. With the amplified signal procedure, this flexible SERS biofilm accomplished sensitive and selective detection of UO 2 2+ ions with a wide linear range from 1 pM to 0.1 μM and a low detection limit of 0.838 pM. This result is nearly five orders below the EPA-defined maximum contaminant level (180 nM). Furthermore, this biofilm gives full play to the advantages of a flexible biosensor. It can directly detect the aquatic products (such as fish and kelp) polluted by UO 2 2+ ions, demonstrating that this flexible SERS biofilm has promising potential for applications in a rapid environmental safety inspection.

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The long non-coding RNA (lncRNA) taurine up-regulated gene 1 (TUG1) acts as tumor-promoting factor in colorectal cancer (CRC). We aimed to elucidate the mechanism by which the transcription factor specificity protein 1 (SP1) regulates TUG1 and microRNAs (miRs)/mRNAs in the context of CRC, which has not been fully studied before. Expression patterns of TUG1 and SP1 were determined in clinical CRC samples and cells, followed by identification of their interaction. Next, the functional significance of TUG1 in CRC was investigated. An in vivo CRC model was established to validate the effect of TUG1. The results demonstrated that TUG1 and SP1 were highly-expressed in CRC, wherein SP1 bound to the TUG1 promoter and consequently, positively regulated its expression. Silencing of TUG1 caused suppression of CRC cell growth and promotion of cell apoptosis. TUG1 could bind to miR-421 to increase KDM2A expression, a target gene of miR-421. TUG1 could activate the ERK pathway by impairing miR-421-targeted inhibition of KDM2A. Additionally, SP1 could facilitate the tumorigenesis of CRC cells in vivo by regulating the TUG1/miR-421/KDM2A/ERK axis. Altogether, the current study emphasizes the oncogenic role of TUG1 in CRC, and illustrates its interactions with the upstream transcription factor SP1 and the downstream modulatory axis miR-421/KDM2A/ERK, thus offering novel insights into the cancerogenic mechanism in CRC.