Nitrogen-doped graphene hydrogels (NGHs) were synthesized through a one-pot hydrothermal route with graphene oxide (GO) as raw material and urea as reducing-doping agents. The morphology, structure, and components of the NGHs were characterized by scanning electron microscopy, Raman spectroscopy, X-ray diffraction, X-ray photoelectron spectroscopy, methylene blue adsorption, thermogravimetric analysis and electrical conductivity measurements. The results demonstrated that nitrogen was doped into the graphene plane at the same time as the GO sheets were reduced, and the nitrogen content incorporated into the graphene lattice was in the range of 3.95 to 6.61 at.% with pyrrolic N as the main component. The NGHs contained about 97.6 wt% water and have a large specific surface area (SSA) of >1300 m 2 g À1 in the wet state. In addition, the electrochemical performance of the NGHs was investigated. The sample NGHs-4 with a nitrogen content of 5.86 at.% and SSA of 1521 AE 60 m 2 g À1 in the wet state showed excellent capacitive behavior (308 F g À1 at 3 A g À1 ) and superior cycling stability (92% retention after 1200 cycles) in 6 mol L À1 KOH. The experimental results indicated that not only the N-content but also the N-type have very significant impact on the capacitive behavior.Furthermore, NGHs strongly influenced the electrochemical properties because of their high SSAs and mesoporous structure.

microRNAs (miRNAs) play critical roles in cancer development and progression. This study investigated the effects of miR-138-5p in human colorectal cancer (CRC) development. miR-138-5p was frequently downregulated in CRC tissues and was associated with advanced clinical stage, lymph node metastasis and poor overall survival. We found that miR-138-5p decreased expression of programmed cell death ligand 1 (PD-L1) through interaction with its PD-L1 3′ untranslated region. miR-138-5p also dramatically suppressed CRC cell growth in vitro and inhibited tumorigenesis in vivo. PD-L1 and miR-138-5p levels were inversely correlated in human CRC tumors, and miR-138-5p inhibited PD-L1 expression in tumor models. These results suggest that miR-138-5p is a tumor suppressor in CRC, and its effects are exerted at least partially through PD-L1 downregulation. Low miR-138-5p and high PD-L1 levels correlated with shorter overall CRC patient survival, indicating that miR-138-5p and PD-L1 may serve as CRC biomarkers for risk group assignment, optimal therapy selection and clinical outcome prediction. Targeting PD-L1, possibly by administering miR-138-5p mimics, might be a clinically effective anti-CRC therapeutic strategy.

The progression of localized breast cancer to distant metastasis results in a poor prognosis and a high mortality rate. In this study, the contributions of miRNAs to tumor progression and the regulatory mechanisms leading to their expression alterations were investigated. Using highly lung-metastatic sub-lines from parental breast cancer cells, miRNA expression profiling revealed that the miR-17-92 cluster is significantly downregulated and the miR-18a-5p is the most evidently decreased. Ectopic expression and inhibition of miR-18a-5p demonstrated its capacity in suppressing migration and invasion of breast cancer cells. Further research identified sterol regulatory element binding transcription protein 1 (SREBP1), the master transcription factor that controls lipid metabolism, as a candidate target of miR-18a-5p. SREBP1 is overexpressed and strongly associated with worse clinical outcomes in breast cancer. Functionally SREBP1 promotes growth and metastasis of breast cancer both in vitro and in vivo. To unravel the underlying mechanism of SREBP1-mediated metastasis, mRNA profiling and subsequent gene set enrichment analyses (GSEA) were performed and SREBP1 was demonstrated to be significantly associated with epithelial-mesenchymal transition (EMT). Furthermore, SREBP1-mediated repression of E-cadherin was found to be deacetylation dependent and was augmented by recruiting Snail/HDAC1/2 repressor complex. In the light of these data, we propose that reduced expression of miR-18a-5p and concomitant overexpression of SREBP1 lead to induction of EMT states that in turn, promote breast cancer progression and metastasis. Taken together, our study reveals the crucial role of miR-18a-5p and SREBP1 in the EMT and metastasis, thus providing promising drug targets for tailored therapy in the advanced breast cancer setting.