Yue Luo

MicroRNAs (miRNAs) regulate gene expression. It has been suggested that obtaining miRNA expression profiles can improve classification, diagnostic, and prognostic information in oncology. Here, we sought to comprehensively identify the miRNAs that are overexpressed in lung cancer by conducting miRNA microarray expression profiling on normal lung versus adjacent lung cancers from transgenic mice. We found that miR-136, miR-376a, and miR-31 were each prominently overexpressed in murine lung cancers. Real-time RT-PCR and in situ hybridization (ISH) assays confirmed these miRNA expression profiles in paired normal-malignant lung tissues from mice and humans. Engineered knockdown of miR-31, but not other highlighted miRNAs, substantially repressed lung cancer cell growth and tumorigenicity in a dose-dependent manner. Using a bioinformatics approach, we identified miR-31 target mRNAs and independently confirmed them as direct targets in human and mouse lung cancer cell lines. These targets included the tumor-suppressive genes large tumor suppressor 2 (LATS2) and PP2A regulatory subunit B alpha isoform (PPP2R2A), and expression of each was augmented by miR-31 knockdown. Their engineered repression antagonized miR-31-mediated growth inhibition. Notably, miR-31 and these target mRNAs were inversely expressed in mouse and human lung cancers, underscoring their biologic relevance. The clinical relevance of miR-31 expression was further independently and comprehensively validated using an array containing normal and malignant human lung tissues. Together, these findings revealed that miR-31 acts as an oncogenic miRNA (oncomir) in lung cancer by targeting specific tumor suppressors for repression.

Bacterial infectious diseases and bacterial-infected environments have been threatening the health of human beings all over the world. In view of the increased bacteria resistance caused by overuse or improper use of antibiotics, antibacterial biomaterials are developed as the substitutes for antibiotics in some cases. Among them, antibacterial hydrogels are attracting more and more attention due to easy preparation process and diversity of structures by changing their chemical cross-linkers via covalent bonds or noncovalent physical interactions, which can endow them with various specific functions such as high toughness and stretchability, injectability, self-healing, tissue adhesiveness and rapid hemostasis, easy loading and controlled drug release, superior biocompatibility and antioxidation as well as good conductivity. In this review, the recent progress of antibacterial hydrogel including the fabrication methodologies, interior structures, performances, antibacterial mechanisms, and applications of various antibacterial hydrogels is summarized. According to the bacteria-killing modes of hydrogels, several representative hydrogels such as silver nanoparticles-based hydrogel, photoresponsive hydrogel including photothermal and photocatalytic, self-bacteria-killing hydrogel such as inherent antibacterial peptides and cationic polymers, and antibiotics-loading hydrogel are focused on. Furthermore, current challenges of antibacterial hydrogels are discussed and future perspectives in this field are also proposed.

In this work, a biomimetic nanozyme catalyst with rapid and efficient self-bacteria-killing and wound-healing performances was synthesized. Through an in situ reduction reaction, a PCN-222 metal organic framework (MOF) was doped with bismuth nanoparticles (Bi NPs) to form Bi-PCN-222, an interfacial Schottky heterojunction biomimetic nanozyme catalyst, which can kill 99.9% of Staphylococcus aureus (S. aureus). The underlying mechanism was that Bi NP doping can endow Bi-PCN-222 MOF with self-driven charge transfer through the Schottky interface and the capability of oxidase-like and peroxidase-like activity, because a large number of free electrons can be captured by surrounding oxygen species to produce radical oxygen species (ROS). Furthermore, once bacteria contact Bi-PCN-222 in a physiological environment, its appropriate redox potential can trigger electron transfer through the electron transport pathway in bacterial membranes and then the interior of the bacteria, which disturbs the bacterial respiration process and subsequent metabolism. Additionally, Bi-PCN-222 can also accelerate tissue regeneration by upregulating fibroblast proliferation and angiogenesis genes (bFGF, VEGF, and HIF-1α), thereby promoting wound healing. This biomimetic enzyme-catalyzed strategy will bring enlightenment to the design of self-bacterial agents for efficient disinfection and tissue reconstruction simultaneously.