ABSTRACT
Objective:To explore the effect of LILRB2 on the proliferation and apoptosis of colorectal cancer SW480 cells, and to further explore its mechanism.Methods:Colorectal cancer SW480 cells were cultured in vitro and divided into blank control group, negative control group and experimental group. The expression of LILRB2 was detected by flow cytometry. The expression of LILRB2 was detected by qPCR, and the empty vector plasmid and the LILRB2 plasmid were transfected into SW480 cells respectively; cell proliferation was detected by CCK-8 method; cell apoptosis was detected by flow cytometry. Western blot was used to detect changes in the expression of related proteins.Results:The expression level of LILRB2 in SW480 was 0.84 ± 0.09, twice higher than that in FHC cells (0.38 ± 0.05) , and the difference was statistically significant ( P<0.05) . After virus infection, the expression of LILRB2 (0.48 ± 0.07) in SW480 cells of the experimental group decreased significantly. CCK-8 experiment results showed that after 12 hours of treatment, the proliferation of SW480 cells in the LILRB2 low expression experimental group was inhibited, and the percentage of apoptosis in SW480 cells in the LILRB2 low expression experimental group increased to 49.3%±1.2%, which was statistically significant ( P<0.05) compared with the percentage of apoptosis in the blank control group and the negative control group (7.48%±0.85%, 7.35%±0.93%) . The ROS level of SW480 cells in the experimental group with low LILRB2 expression was significantly higher than that in the blank control group and negative control group ( P<0.05) . After adding ROS scavenger NAC, the apoptosis of LILRB2 in the experimental group increased. Conclusion:The low expression of LILRB2 inhibits the proliferation of SW480 cells and induces apoptosis, which may play a role by regulating the level of ROS, providing a theoretical basis for the study of LILRB2 in colorectal cancer.
ABSTRACT
Bacterial multi-drug resistance (MDR) is a global challenge in the fields of medicine and health, agriculture and fishery, ecology and environment. The cross-region spread of antibiotic resistance genes (ARGs) among different species is one of the main cause of bacterial MDR. However, there is no effective strategies for addressing the intensifying bacterial MDR. The CRISPR-Cas system, consisting of clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR associated proteins, can targetedly degrade exogenous nucleic acids, thus exhibiting high application potential in preventing and controlling bacterial MDR caused by ARGs. This review briefly introduced the working mechanism of CRISPR-Cas systems, followed by discussing recent advances in reducing ARGs by CRISPR-Cas systems delivered through mediators (e.g. plasmids, bacteriophages and nanoparticle). Moreover, the trends of this research field were envisioned, providing a new perspective on preventing and controlling MDR.