ABSTRACT
Fabricating insoluble and infusible porous materials into gels for advanced applications is of great importance but has formidable challenges. Here, we present a general, facile, and scalable protocol to fabricate covalent organic framework (COF) gels using a group-protection synthesis strategy. To prove the generality of this strategy, we successfully prepared 10 types of COF organohydrogels with high crystallinity, porosity, good mechanical properties, and excellent solvent and freezing resistance. Notably, these COF organohydrogels can easily transform into hydrogels, organogels, and aerogels, breaking the gaps between different types of COF gels. An in-depth mechanism investigation unveils that the group-protection strategy effectively slows down the formation rate and regulates the morphology of COFs, benefiting the formation of cross-linked nanofibers/nanosheets to produce COF gels. We also find that the hydrogen bond network formed by the organic/water binary solvent and functional groups in the COF skeletons plays a vital role in creating organohydrogels and maintaining frost resistance and solvent resistance. As an application demonstration, COF gels installed with photoresponsive azobenzene groups show excellent solar energy absorption, photothermal conversion, and water transmission performances, demonstrating great potential in solar desalination. This work enriches the synthesis toolboxes for COF gels and expands the application scope of COFs.
ABSTRACT
LINC00467 was reported as an oncogenic gene in different types of human cancers. In this study, we investigated the molecular mechanisms of LINC00467 in the tumorigenesis of laryngeal squamous cell cancer (LSCC). RT-qPCR was utilized to detect the mRNA expression of genes, and western blot assay was used to determine the protein levels of TNF alpha-induced protein 3 (TNFAIP3). The cell viability was detected by CCK-8 assay. Transwell assays were conducted to determine the cell migration and invasion of LSCC cells, and the cell cycle was assessed by flow cytometry. The association between paired box 5 (PAX5), LINC00467, miR-4735-3p, and TNFAIP3 was verified using ChIP, RNA pull-down, or luciferase reporter assays. In our study, we found that LINC00467 was upregulated in LSCC, and knockdown of LINC00467 suppressed cell viability and metastasis of LSCC. Besides, LINC00467 transcription could be activated by PAX5 in LSCC. Furthermore, LINC00467 acted as competitive endogenous RNA (ceRNA) for miR-4735-3p to accelerate LSCC progression. In the meantime, TNFAIP3 was identified as a downstream gene of miR-4735-3p. Finally, TNFAIP3 overexpression could overturn the effects of miR-4735-3p mimic on LSCC cellular activities. In conclusion, our results demonstrated that PAX5-induced LINC00467 facilitated LSCC progression by inhibiting miR-4735-3p to increase TNFAIP3 expression.
