Long non-coding RNA MIR155HG knockdown suppresses cell proliferation, migration and invasion in NSCLC by upregulating TP53INP1 directly targeted by miR-155-3p and miR-155-5p.

OBJECTIVE: Previous studies have proved that lncRNA MIR155 host gene (MIR155HG) is overexpressed in glioma and has elucidated its function. However, its functional role and underlying molecular mechanism in non-small cell lung cancer (NSCLC) are unknown. This study aimed to investigate the function and underlying mechanism of MIR155HG in NSCLC. MATERIALS AND METHODS: Differentially expressed lncRNAs in NSCLC tissue were identified from Gene Expression Omnibus (GEO) database. The expression of MIR155HG, miR-155-3p, miRNA-155-5p, and tumor protein p53-inducible nuclear protein 1 (TP53INP1) in NSCLC specimens and cells were quantified using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blotting analysis. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and transwell invasion assay were performed to evaluate cell viability and the ability of migration and invasion. Luciferase reporter assay was employed to examine whether miR-155-3p and miR-155-5p could bind to TP53INP1 in NSCLC cells. A xenograft tumor model was used to evaluate the biological function of MIR155HG in vivo. RESULTS: Data obtained from the GEO dataset show that MIR155HG is frequently overexpressed in NSCLC tumor tissues and cell lines. Elevated MIR155HG levels were found to be associated with advanced disease stage and poor prognosis of NSCLC. Cell viability, as well as the capability of migration and invasion of NCI-H1975 and A549 cells, was markedly reduced upon MIR155HG knockdown. Mechanistically, bioinformatics analysis and functional assays confirmed that miR-155-5p and miR-155-3p, two derivatives of MIR155HG, contributed to the effect of MIR155HG in NSCLC. It was also found that miR-155-5p or miR-155-3p mimics could dramatically rescue the inhibition of cell proliferation, migration, and invasion caused by siMIR155HG. Furthermore, bioinformatics analysis and Luciferase reporter assays revealed that miR-155-5p and miR-155-3p mediate the effect of MIR155HG in NSCLC cells by negatively regulating the tumor suppressor TP53INP1. CONCLUSIONS: Current findings indicate that MIR155HG/miR-155 axis facilitates NSCLC progression by downregulating TP53INP1. Therefore, the MIR155HG/miR-155 axis may be a potential therapeutic target for NSCLC.

Relations of hepatic steatosis with liver functions, inflammations, glucolipid metabolism in chronic hepatitis B patients.

OBJECTIVE: To investigate the relations between the steatosis and liver functions, inflammations, and glucolipid metabolism in chronic hepatitis B patients. PATIENTS AND METHODS: A total of 144 chronic hepatitis B patients who were admitted to our hospital from January 2015 to April 2017 were selected and divided into the steatosis group (n=73) and the non-steatosis group (n=71) according to the detection of hepatic puncture biopsy. The general information of the patients including age, sex, and body mass index (BMI) was collected, and patients' liver functions, inflammations, and glucolipid metabolism indicators were determined and compared between the chronic hepatitis patients with steatosis and without steatosis. The chronic hepatitis patients with steatosis were further divided into the normal group and the abnormal group based on the level of C-reactive protein (CRP) (8 mg/L). Besides, according to the level of aspartate aminotransferase (AST), these patients were divided into the normal liver function group (AST<40 U/L) and the abnormal liver function group (AST>40 U/L), among whom the hepatic steatosis, glucolipid metabolism, and inflammations were compared. At the same time, the chronic hepatitis B patients with steatosis were divided into Group F1, Group F2, and Group F3 based on the fatty degeneration grade, the correlations of steatosis with inflammations, glucolipid metabolism, and liver functions were analyzed. At last, the regression analyses between steatosis and the inflammation grade, glucolipid metabolism and liver function indicators were conducted for Group F1, F2, and F3, respectively. RESULTS: In the chronic hepatitis B patients with steatosis, liver function indicators-alanine aminotransferase (ALT) and AST, levels of inflammatory factors-interleukin-2 (IL-2), IL-6 and CRP and glucolipid metabolism indicators-fasting blood glucose (FBG), 2h postprandial blood glucose (2h PBG), fasting insulin (FINS), triacylglycerol (TG), total cholesterol (TC), and low-density lipoprotein (LDL) were significantly higher than those without steatosis (p<0.05). The steatosis, liver functions, and glucolipid metabolism indicators were statistically different between patients in the normal inflammatory factor group and the abnormal inflammatory factor group (p<0.06). In addition, the liver function indicators (ALT and AST) and glucolipid metabolism indicators (FBG, 2h PBG, FINS, TG, TC, HDL, and LDL) in the abnormal group were statistically higher than those of normal inflammatory factor group (p<0.05). In the normal liver function group, the average fatty degeneration grade was statistically lower than that in the abnormal liver function group (p<0.05), and glucolipid metabolism indicators (FBG, 2h PBG, FINS, TG, TC, IL-2, IL-6, CRP, HDL, and LDL) were also markedly lower than those in the abnormal liver function group (p<0.05). The steatosis was positively correlated with relevant indicators, including the blood glucose indicator of FBG (r=0.509, p<0.05), liver function indicator of AST (r=0.602, p<0.05), the blood lipid indicator of TG (r=0.740, p<0.05), and the inflammatory factor of CRP (r=0.882, p<0.05), respectively. The disease course, BMI, 2h FBG, FINS, TG, TC, HDL, LDL, AST, ALT, and inflammatory factors of IL-2, IL-6, and CRP were involved in risk factors of steatosis (p<0.05). CONCLUSIONS: Our data demonstrates that the steatosis is correlated with liver functions, glucolipid metabolism and inflammation level in chronic hepatitis B patients, and the foregoing indicators can affect the disease development of chronic hepatitis B patients with steatosis.

EFFECT OF PREGNANE XENOBIOTIC RECEPTOR ACTIVATION ON INFLAMMATORY BOWEL DISEASE TREATED WITH RIFAXIMIN.

The causes and pathogenesis of Inflammatory Bowel Disease (IBD) are still not clearly understood. This study aims to prove the important role of rifaximin played in inflammatory reaction caused by abnormity of the intestinal mucosal immune system. Intestinal microflora can greatly promote and maintain the inflammatory reaction of IBD, therefore, antibiotics can be used to treat IBD. Rifaximin is a medicine usually used for local intestinal infection. Many clinical and basic studies have shown that both a single application of rifaximin and the joint application with other medicines could achieve a good efficacy. This paper studied the activation of Pregnane Xenobiotic Receptor (PXR) in treating IBD with rifaximin and analyzed its efficacy in IBD when PXR was involved in the transport of medicine and metabolism. The results prove that rifaximin can not only serve as an anti-microbial drug, but can activate PXR and actually weaken the reaction of IBD. Thus it is safe to say that rifaximin has great potential in treating IBD.

MRI appearance of multiple eccrine spiradenoma.

Multiple eccrine spiradenoma is one of the rarest tumours of the sweat gland. We report a case of multiple eccrine spiradenoma that was distributed in several parts of the body. On MRI the lesions presented with multiple dispersive foci with clear circumferences in the cutis and the subcutaneous tissue. The lesions showed low signal intensity on T1 weighted images, and high signal intensity on short tau inversion recovery images. Although the signal intensities of the lesions were not characteristic in this patient, multiple eccrine spiradenoma should be included in the differential diagnosis of the lesions in the cutis and the subcutaneous tissue.