Bioinformatics analysis of sterol O⁃acyltransferase 1 gene related to hepatocellular carcinoma / 中国生物制品学杂志

@#Abstract：Objective To predict the structure and function of sterol O⁃acyltransferase 1（SOAT1）related to hepatocellular carcinoma（HCC）by using bioinformatics tools，in order to understand its mechanism as the marker and therapeutic target of S⁃Ⅲ subtype. Methods The structure，function and protein interaction of SOAT1 were predicted and analyzed by using databases or softwares such as NCBI，STRING，Protscale，SignalP，TMHMM，PSORT，SOPMA，SWISS ⁃ MODEL， NetNGlyc，NetOGlyc，Netphos and ProtParam. Results The protein encoded by SOAT1 was a hydrophobic protein with good stability，which was a nonclassical pathway protein with 8 transmembrane regions，mainly distributed among the cell membrane. SOAT1 was expressed in many tissues，while most of them in the adrenal gland，which showed multiple phosphorylation sites and was mainly involved in the synthesis and catabolism of cholesterol. Conclusion Bioinformatics analysis of structure and function of SOAT1 showed that SOAT1 lipid synthesis and catabolism pathways played an important role，and lipid expression was closely related to the development of cancer，indicating that the treatment of HCC may be achieved by regulating the expression of SOAT1 gene.

LncRNA SOX2OT Mediates Mitochondrial Dysfunction in Septic Cardiomyopathy.

Researches establish an indispensable role of mitochondrial dysfunction in septic cardiomyopathy. We aimed to investigate the effects of long noncoding RNA (LncRNA) SOX2 overlapping transcript (SOX2OT) on mitochondrial dysfunction in septic cardiomyopathy. We observed an obvious overexpression of SOX2OT in septic hearts and cardiomyocytes. Knockdown of SOX2OT in mice recovered the reduced cardiac function, and improved the mitochondrial membrane potential impaired by lipopolysaccharide (LPS). SOX2OT overexpressed mice showed the opposite situation. In parallel, knockdown of SOX2OT in cardiomyocytes restored the mitochondrial membrane potential, along with reduced mitochondrial reactive oxygen species production induced by LPS, while overexpression of SOX2OT reversed these effects. Mechanistically, SOX2OT could regulate mitochondrial dysfunction in septic cardiomyopathy via SOX2. In general, SOX2OT contributed to mitochondrial dysfunction progression via inhibiting SOX2 expression in septic cardiomyopathy, which may provide a new insight for treatment of septic cardiomyopathy.