Current treatments for chronic diabetic wounds remain unsatisfactory due to the lack of ideal wound dressings that can integrate matching mechanical strength, fast self‐healability, facile dressing change, and multiple therapeutic effects into one system. In this work, benefiting from the catechol groups and therapeutic effect of epigallocatechin‐3‐gallate (EGCG, green tea derivative), a smart hydrogel dressing can be conveniently obtained through copolymerization of the complex formed by EGCG and 3‐acrylamido phenylboronic acid (APBA) (the formation of boronate ester bond) and acrylamide. The resulting hydrogel features adequate mechanical properties, self‐healing capability, and tissue adhesiveness. Otherwise, the substantial release of EGCG can not only realize anti‐oxidation, antibacterial, anti‐inflammatory and proangiogenic effect, and modulation of macrophage polarization to accelerate wound healing, but also facilitate easy dressing change. This advanced hydrogel provides a facile and effective way for diabetic chronic wound management and may be extended for the therapy of other complicated wound healings.

Prostate cancer (PCa) is one of the major men’s malignancies with high mortality worldwide. Circular RNAs (circRNAs) have been shown to serve as essential regulators in human cancers. CircRNA can exert their functions by cooperating with their host genes. In the present study, microarray analysis revealed an upregulated mRNA in PCa samples. X-linked inhibitor of apoptosis protein (XIAP), a key regulator in the progression of human cancers. Through bioinformatics analysis, we determined that XIAP is a host gene for circRNA0005276. Therefore, this study focused on the interaction between circ0005276 and XIAP as well as their functions in PCa progression. The upregulation of XIAP and circ0005276 was determined in PCa tissues and cell lines. Moreover, we confirmed the positive regulation of circ0005276 on XIAP expression. Functionally, we validated that circ0005276 and XIAP promoted cell proliferation, migration and epithelial–mesenchymal transition. Mechanistically, we verified that circ0005276 interacted with FUS binding protein (FUS) so as to activate the transcription of XIAP. Rescue assays were conducted to determine the crucial role of XIAP in circ0005276 and FUS-mediated PCa cellular processes. Collectively, our study revealed the mechanism and function of circ0005276 and its host gene XIAP in PCa progression.

Curcumin is known to exhibit anticancer effects on various cancers with selective cytotoxicity in tumor cells. In the present study, the effects of curcumin‑induced multiple PCDs on human non‑small cell lung cancer (NSCLC) cells and the potential molecular mechanisms of apoptosis and autophagy triggered by curcumin via the PI3K/Akt/mTOR signaling pathway were explored, further confirmed by co‑culture of curcumin with mTOR blocker rapamycin and PI3K/Akt inhibitor LY294002. The anti‑proliferation effect of different stimulus was measured by MTT assay. Apoptosis was detected by flow cytometry. Autophagy induction was detected by MDC labeling and western blotting of Beclin1, LC3, and p62 expression. The mRNA and protein expression levels of Akt and mTOR were assayed by real‑time fluorescence quantitative (qRT‑PCR) technique and western blotting. Our results showed that curcumin inhibited the viability of A549 cells time‑ and dose‑dependently. In addition, a dosage-dependent A549 cell apoptosis‑induction phenomena was observed by the curcumin intervention. Moreover, obvious autophagy was induced after curcumin‑treatment, characterized by the formation of fluorescent particles [autophagic vesicles (AVs)] and significant increase in ratio of LC3‑Ⅱ/LC3‑Ⅰ and Beclin1 as well as decreased p62 expression. Furthermore, the effect of curcumin on a substantial downregulation of phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway was observed. It is worth noting that the inhibition of mTOR by rapamycin or of PI3K/Akt by LY294002 augmented curcumin‑induced apoptosis and autophagy, leading to significant inhibition of cell proliferation. From these findings, it can be speculated that curcumin potently inhibit the cell growth of NSCLC A549 cells through inducing both apoptosis and autophagy by inhibition of the PI3K/Akt/mTOR pathway. These results support the potential use of curcumin as a novel candidate in treatment of human lung cancer.

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