Nanomaterials with Glucose Oxidase-Mimicking Activity for Biomedical Applications.

Glucose oxidase (GOD) is an oxidoreductase that catalyzes the aerobic oxidation of glucose into hydrogen peroxide (H2O2) and gluconic acid, which has been widely used in industrial raw materials production, biosensors and cancer treatment. However, natural GOD bears intrinsic disadvantages, such as poor stability and a complex purification process, which undoubtedly restricts its biomedical applications. Fortunately, several artificial nanomaterials have been recently discovered with a GOD-like activity and their catalytic efficiency toward glucose oxidation can be finely optimized for diverse biomedical applications in biosensing and disease treatments. In view of the notable progress of GOD-mimicking nanozymes, this review systematically summarizes the representative GOD-mimicking nanomaterials for the first time and depicts their proposed catalytic mechanisms. We then introduce the efficient modulation strategy to improve the catalytic activity of existing GOD-mimicking nanomaterials. Finally, the potential biomedical applications in glucose detection, DNA bioanalysis and cancer treatment are highlighted. We believe that the development of nanomaterials with a GOD-like activity will expand the application range of GOD-based systems and lead to new opportunities of GOD-mimicking nanomaterials for various biomedical applications.

Effect of Trace Element Selenium on the Intestinal Microbial Community in Nude Mice with Colorectal Cancer.

Colorectal cancer (CRC) is the third most common cancer worldwide. The role of intestinal microbiota in carcinogenesis has also become an important research topic, and CRC is closely related to the intestinal microbiota. Selenium-containing compounds have attracted more attention as anticancer drugs as they can have minimal side effects. The purpose of this study was to determine and compare the effect of sodium selenite and selenomethionine on the microbial communities of nude mice with CRC. A CRC ectopic tumorigenesis model was established by subcutaneously injecting HCT116 cells into nude mice. The mice were then intraperitoneally injected with sodium selenite and selenomethionine for 24 days to regulate their intestinal microbiota. Compared with sodium selenite, selenomethionine resulted in a greater reduction in the richness and diversity of intestinal microbiota in nude mice with CRC, and the richness and diversity were closer to healthy levels. Selenomethionine also regulated a wider variety of flora. Additionally, sodium selenite and selenomethionine produced different microorganisms, changed function and metabolic pathways in the intestinal microbiota. Both sodium selenite and selenomethionine have certain effects on restoring the intestinal microbial diversity in nude mice with CRC, and the effect of selenomethionine is better than that of sodium selenite.

Research on the Effect and Mechanism of Selenium on Colorectal Cancer Through TRIM32.

The intake of selenium (Se) in the human body is negatively correlated with the risk of colorectal cancer (CRC), but its mechanism in the occurrence and development of CRC is not clear. This study aimed to evaluate the therapeutic effect of Se on CRC, and explore the anti-tumor effect of Se supplementation on CRC and its molecular mechanism. In this study, we utilized colony formation assay, cell scratch test, Transwell migration, and flow cytometry to assess cell proliferation, migration, and apoptosis. Our findings demonstrate that Se effectively suppresses the growth and proliferation of CRC cell lines HCT116 and SW480 and promoting cellular apoptosis. In vivo experiments demonstrated a significant inhibitory effect of Se on tumor growth. CRC-related datasets were extracted from the Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases for differential expression analysis of TRIM32 and survival analysis. We found that TRIM32 was highly expressed in tumor tissues of CRC patients and correlated with a poor prognosis. Furthermore, through RNA sequencing analysis, we identified TRIM32 as a gene that was significantly decreased after Se treatment in HCT116 cells. This finding was subsequently validated by Western blot results. Moreover, TRIM32 knockdown combined with Se treatment significantly inhibited cell growth proliferation and migration and further induced apoptosis of colorectal cancer cells. In conclusion, our findings provided evidence that Se inhibited the growth of colorectal cancer cells by down-regulating TRIM32.

LncRNA MEG3 inhibits the development of nasopharyngeal carcinoma by sponging miR-543 targeting KLF4.

BACKGROUND: Emerging evidence shows that long non-coding RNAs (lncRNAs) play a crucial role in tumor development by regulating biological behavior in various cancer cells. Several lncRNAs act as miRNA sponges by binding miRNA sequences and thus regulating mRNA expression. The lncRNA maternally expressed gene 3 (MEG3) has decreased expression levels in many cancer cells and acts as a tumor suppressor in different cancers. MEG3 also showed decreased expression in nasopharyngeal carcinoma (NPC) and plays a role in tumor suppression; however, the detailed mechanism of tumor suppression in NPC cells has not been reported. This paper aimed to explore the function and molecular mechanisms of MEG3 in the development of NPC. METHODS: MEG3 and miR-543 levels in NPC cells were detected by quantitative real-time PCR (qRT-PCR). The regulatory role of MEG3 in NPC cells was examined using knockdown and overexpression of MEG3 in C666-1 cells. Cell proliferation was analyzed by the cell counting kit-8 (CCK-8) assay, cell migration and invasion capacities were evaluated using Transwell assay, and cell apoptosis was assessed using flow cytometry. The relationship between MEG3 and miR-543 was investigated by luciferase reporter assay. MEG3- and Krüppel like factor 4 (KLF4)-mediated changes in NPC cell proliferation and apoptosis were analyzed, and KLF4, Bcl-2 and Bax protein expression levels were measured by western blotting. RESULTS: The results showed that MEG3 was decreased and miR-543 was increased in NPC cell lines, and upregulated MEG3 inhibited cell proliferation, migration, and invasion and promoted apoptosis, suggesting that MEG3 acts as a tumor suppressor in NPC cells. Furthermore, a luciferase reporter assay and western blotting indicated that MEG3 regulated KLF4 expression by sponging miR-543. Functionally, overexpression of MEG3 suppressed cell proliferation, promoted cell apoptosis and affected Bcl-2 and Bax protein levels via regulation of KLF4 expression mediated by sponging miR-543. CONCLUSIONS: These findings show that lncRNA MEG3 inhibits the development of NPC by sponging miR-543 targeting KLF4 and that MEG3 can serve as a new novel target for NPC therapeutics.