Hydrogels with injectability and robustness have great promise in clinical practice. However, current injectable hydrogels are usually mechanically weak. Here, an idea, "preformed hydrogel reversion", is proposed to develop robust injectable hydrogels through an intermediate unit-mediated, continuous structural inheritance strategy. In this strategy, robust preformed hydrogels are physically disassembled into intermediate injectable structure-inherited microgels (SIMs), and upon encountering water in physiological environment, the SIMs can construct a macroscopical robust structure with the driving force of hydrogen bonds (H-bonds). The physical disassembly and construction process enables the inheritance of robust structures through SIMs, thereby realizing both excellent injectability and robustness. Beyond that, the SIMs also exhibit long-term storage stability and convenient usability. Using protein drug loading and hemostasis as examples, it is demonstrated that the SIM system shows superiorities in biomedical applications. The proposed idea of "preformed hydrogel reversion" can open new horizons for developing robust injectable hydrogels for diverse applications.

Hepatocellular carcinoma (HCC) is a common malignant liver tumor worldwide. Tumor recurrence and metastasis contribute to the bad clinical outcome of HCC patients. Substantial studies have displayed lncRNAs modulate various tumorigenic processes of many cancers. Our current work was aimed to investigate the function of LINC00675 in HCC and to recognize the potential interactions between lncRNAs and microRNAs. GFI1 can exhibit a significant role in the progression of human malignant tumors. Firstly, GFI1 was identified using real-time PCR in HCC tissues and cells. In this work, we indicated GFI1 was remarkably reduced in HCC tissues and cells. Meanwhile, GFI1 specifically interacted with the promoter of LINC00675. Up-regulation of LINC00675 obviously repressed the migration and invasion capacity of SMCC-7721 and QGY-7703 cells in vitro. Moreover, decrease of LINC00675 competitively bound to miR-942-5p that contributed to the miRNA-mediated degradation of GFI1, thus facilitated HCC metastasis. The ceRNA function of LINC00675 in HCC cells was assessed and confirmed using RNA immunoprecipitation assay and RNA pull-down assays in our work. Additionally, we proved overexpression of miR-942-5p promoted HCC progression, which was reversed by the up-regulation of GFI1. In summary, LINC00675 might act as a prognostic marker for HCC, which can inhibit HCC development via regulating miR-942-5p and GFI1.

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. MicroRNAs (miRNAs) are a group of endogenous small non-coding RNAs that regulate target genes, and play a critical role in many biological processes. However, the underlying mechanism of specific miRNA, miR-130a-3p, in AS remains largely unknown. Therefore, the present study aimed to explore the underlying mechanism of miR-130a-3p in the development of AS. In the present study, it was revealed that miR-130a-3p was downregulated in T cells from HLA-B27-positive AS patients compared with the HLA-B27-negative healthy controls. Next, bioinformatics software TargetScan 7.2 was used to predict the target genes of miR-130a-3p, and a luciferase reporter assay indicated that HOXB1 was the direct target gene of miR-130a-3p. Furthermore, it was determined that HOXB1 expression was upregulated in T cells from HLA-B27-positive AS patients. In addition, the results of the present study indicated that miR-130a-3p inhibitor significantly inhibited cell proliferation ability and induced cell apoptosis of Jurkat T cells, while the miR-130a-3p mimic promoted proliferation ability and inhibited cell apoptosis of Jurkat T cells. Notably, all the effects of the miR-130a-3p mimic on Jurkat T cells were reversed by HOXB1-plasmid. Collectively, our data indicated that miR-130a-3p was decreased in T cells from AS patients and it could regulate T-cell survival by targeting HOXB1.

Accumulating evidence indicates that circular RNAs (circRNAs) can interact with microRNAs to modulate gene expression in various cancers, including hepatocellular carcinoma (HCC). Although the significant role of circRNAs has been well documented in HCC, the complex mechanisms of circRNAs still need to be elucidated. Our current study is aimed at investigating the function of circ_0001588 in HCC, which was observed to significantly increase in HCC tissues and cells. We demonstrated that the knockdown of circ_0001588 resulted in repressed cell proliferation, migration, and invasion. In vivo studies using a nude mouse model showed that circ_0001588 downregulation reduced tumor size. Moreover, miR-874 was predicted as a target of circ_0001588. Using luciferase binding assays, we proved that circ_0001588 functions as a molecular ceRNA of miR-874 and that CDK4 acts as a downstream target of miR-874 in HCC. It was confirmed that overexpression of miR-874 decreased the proliferation, migration, and invasion triggered by the increase in circ_0001588. In summary, our results indicate that circ_0001588 acts as a ceRNA and promotes HCC progression by targeting the miR-874/CDK4 signaling pathway. Hence, we propose that circ_0001588 may be a promising target for HCC treatment.

No abstract