Modifying thin film composite membrane with zeolitic imidazolate framework-8@polydopamine for enhanced antifouling property.

Biofouling and organic fouling are major obstacles for polymeric membranes during application. In this work, zeolitic imidazolate framework-8@polydopamine (ZIF-8@PDA) nanoparticles were prepared by an aqueous synthesis strategy and incorporated into the polyamide (PA) selective layer to synthesize thin film nanocomposite membrane (TFN) during interfacial polymerization. The permeability and selectivity of the composite membrane were simultaneously improved with the introduction of ZIF-8@PDA. The water permeability of the TFN membrane increased to 3.74 ± 0.19 L/(m2·h·bar), which is 43.8% higher than that of the control membrane. Besides, the rejection of TFN membrane to sodium chloride is 98.68 ± 0.13%, which shows 0.99% increment than the unmodified membrane. Moreover, organic fouling and biofouling of the TFN membrane were also alleviated thanks to the introduction of the hydrophilic ZIF-8@PDA. The short-term filtration results indicate the performance of the TFN membrane is stable during operation.

Facile microwave-assisted synthesis of In2O3 nanocubes and their application in photocatalytic degradation of tetracycline.

Novel In2O3 nanocube photocatalysts were successfully prepared by a facile microwave-assisted synthesis method. The obtained products are nano-sized with square corners and high crystallinity. The In2O3 nanocubes possessed high efficiency of electron-hole separation, resulting in high photocatalytic activities for the degradation of tetracycline under both visible light (λ > 420 nm) and full-range light irradiation (360-760 nm), the ratios of which are 39.3% and 61.0%, respectively. Moreover, the calculated positions of the CB and VB under our experimental conditions at the point of zero for In2O3 nanocubes are -0.60 V and +2.17 V, respectively. Note that the redox potentials of [O2/·O2 -] and [·OH/OH-] are -0.33 V and +2.38 V, respectively, which means that the irradiated In2O3 nanocubes can reduce O2 into ·O2 - without oxidizing OH- into ·OH. It can be concluded that ·O2 - and h+ are the main active species of In2O3 in aqueous solution under visible light irradiation and full-range light irradiation.

[Sunitinib suppresses migration of ovarian cancer cells through negative modulation of TGF-ß-mediated epithelial-mesenchymal transition].

OBJECTIVE: To investigate the effect of sunitinib on the migration of ovarian cells and its mechanism of the negative regulation TGF-ß mediated of epithelial-mesenchymal transition(EMT) by sunitinib to inhibit ovarian cancer metastasis. METHODS: The migration of human ovarian cancer cells SKOV3 was evaluated by wound-healing and transwell assays. The effects of sunitinib on TGF-ß-induced E-cadherin expression was assessed by Western-blotting, real time RT-PCR and immunofluorescence assay. The protein levels of Snail and the transcriptional activity of Smad in sunitinib-treated cells were examined by Western-blotting and SBE-luciferase assay. RESULTS: Sunitinib suppressed the migration of SKOV3 cells in a concentration-dependent manner. TGF-ß stimulation reduced E-cadherin protein level, which was attenuated by sunitinib. Sunitinib inhibited the up-regulation of Snail protein level induced by TGF-ß treatment. The SBE reporter was constructed by linking the Smad-binding elements promoter upstream of luciferase reporter gene. A remarkable increment of transcriptional activity of Smads complexes was observed in SKOV3 cells exposed to TGF-ß, which was significantly prohibited by sunitinib. CONCLUSION: Sunitinib can inhibit the migration of SKOV3 cells and attenuate the down-regulation of E-cadherin protein level induced by TGF-ß. Sunitinib can abolish TGF-ß-induced up-regulation of Snail protein and decrease the transcriptional activity of Smad complexes. The results indicate that sunitinib suppresses migration of ovarian cancer cells through negative modulation of TGF-ß-mediated epithelial-mesenchymal transition.

Small ubiquitin-related modifier-1 modification regulates all-trans-retinoic acid-induced differentiation via stabilization of retinoic acid receptor α.

Small ubiquitin-related modifier-1 (SUMO-1) modification has been implicated in many important cellular processes, including cell cycle progression, apoptosis, cellular proliferation, and development, but its role in all-trans-retinoic acid (ATRA)-induced differentiation processes of cancer cells remains unclear. Here, we report for the first time that ATRA-induced differentiation of leukemia and osteosarcoma is accompanied by a decrease in the level of SUMO-1 protein. Our results also demonstrated that depletion or inhibition of SUMO-1 blocks ATRA-induced differentiation, suggesting that SUMO-1 is critical for the differentiation effect of ATRA. Further studies indicated that SUMO-1-promoted ATRA-induced differentiation might be associated with the stabilization of retinoic acid receptor α (RARα), protecting it from degradation. Moreover, our results suggested that Lys399 is a major site for SUMO-1 conjugation of RARα. We also found that RARα enhanced the transcription of its target genes, which might also contribute to the enhanced differentiating effects of ATRA; however, mutation of Lys399 of RARα inhibits the extents of both SUMO-1 modification and ATRA-induced differentiation. Together, these results indicate that SUMO-1 modification of RARα is a potent mechanism for balancing proliferation and differentiation by controlling the stability of RARα in cancer cells. SUMO-1 modification may thus serve an important role in controlling ATRA-induced cell differentiation in cancers.