ABSTRACT
OBJECTIVE: The composition of microbiota which correlates with infiltrating immune cells and clinical signatures is not clarified in CRC. METHODS: We applied 4 kinds of bioinformatic tools GSVA (version: 1.42.0), ESTIMATE (version: 1.0.13), CIBERSORT (version: 2.0), and immune-related genes. RESULTS: We found that a total of 8 types of microbiotas appeared in the three immune correlation analyses. Among these microbiotas, significant enrichments in relative abundances associated with immune cell infiltration can be found for the dominant phyla Proteobacteria, Firmicutes, and Actinobacteria. Moreover, there existed correlations between some of the 8 microbiotas and clinical-related indicators. CONCLUSION: We identified some novel microbiotas involved in immune regulation in CRC.
ABSTRACT
ABSTRACT: Myocardial ischemia-reperfusion injury (MIRI) is a vital risk factor for cardiovascular diseases. Some circular RNAs (circRNAs) have been identified as modulators of MIRI. But, the effects of circ-mitochondrial amidoxime reducing component 2 (circ-MARC2) in MIRI are unclear. Our results showed that circ-MARC2 was overexpressed in hypoxia/reoxygenation (H/R)-treated AC16 cells. Circ-MARC2 silencing reversed the inhibitory effect of H/R treatment on cell proliferation and promoting effects on lactate dehydrogenase (LDH) activity, creatine kinase (CK-MB) activity and cell apoptosis in AC16 cells. Moreover, circ-MARC2 served as the sponge for miR-335-5p and ameliorated H/R-induced AC16 cell damage by decoying miR-335-5p. Additionally, transient receptor potential cation channel subfamily M member 7 (TRPM7) was identified as the target gene of miR-335-5p. Overexpression of miR-335-5p relieved H/R-induced AC16 cell damage, while TRPM7 elevation abolished the effect. Circ-MARC2 knockdown was able to relieve H/R-induced AC16 cell injury through miR-335-5p/TRPM7 axis.
