circNFIX facilitates hepatocellular carcinoma progression by targeting miR-3064-5p/HMGA2 to enhance glutaminolysis.

Hepatocellular carcinoma (HCC) is acknowledged to be a fatal malignant cancer around the world. Circular RNAs (circRNAs) function as crucial regulators in the pathological procession of HCC. Here, we elucidated the biological function of a novel circRNA, circNFIX, in HCC tumorigenesis. qRT-PCR was performed to determine the expressions of circNFIX, miR-3064-5p, and HMGA2. circNFIX stability was evaluated after treatment with ribonuclease R. The growth and invasion of HCC cells were assessed by CCK8 and transwell assays. Protein levels were measured by Western blotting. The levels of glutaminolysis metabolites were evaluated by commercial kits. Dual-luciferase report assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were performed for validating the interaction between miR-3064-5p and circNFIX/HMGA2. Tumor growth in vivo was detected using xenograft assay. Our results showed that circNFIX was remarkably up-regulated in HCC and was associated with a poor survival. Knockdown of circNFIX repressed proliferation, invasion and glutaminolysis of HCC cells. Moreover, circNFIX directly sponged miR-3064-5p to release HMGA2 expression, and thus conferred the malignant development of HCC. In conclusion, circNFIX serves as a competing endogenous RNA to accelerate HCC progression via regulating miR-3064-5p/HMGA2 axis, suggesting a therapeutic strategy for HCC intervention.

[Adefovir dipivoxil effects on and related factors of blood phosphorus metabolism in patients with chronic hepatitis B].

OBJECTIVE: To investigate the effects of adefovir dipivoxil (ADV) on blood phosphorus metabolism in patients with chronic hepatitis B (CHB). METHODS: Patients with hepatitis B surface antigen (HBsAg)-positive CHB were treated with ADV alone, ADV combined with interferon (IFN), or ADV combined with lamivudine (LAM). Changes in levels of calcium, phosphate, urea, and creatinine were assessed at treatment weeks 4, 12, 24, 48, 72 and 96. Statistical analysis was carried out with SPSS 16 software; influential factors were analyzed by ANOVA and non-conditional logistic regression analysis. RESULTS: During the course of treatments, 32 (42.6%) of the patients presented with low phosphorus. The highest incidence of low phosphorus was found to have occurred at treatment week 24 (25.0%, 27.5% and 36.4% respectively, with no statistical difference between three groups, x2=0.225, P>0.225). Patients with hypophosphatemia did not show a significant difference in serum phosphorus levels from the other patients (F=1.853, P=0.169). Logistic regression showed a correlation between low phosphorus and sex (x2=7.876, P<0.05), age (t=2.479, P<0.05), and serum creatinine (t =-2.256, P<0.05), but not with blood urea nitrogen or blood calcium (P>0.05). CONCLUSION: ADV antiviral treatment can decrease the blood phosphorous levels of CHB patients, particularly over extended time of treatment, and the occurrence of low phosphorus is more common than of mild phosphorus decrease.Male and elderly patients may be at greater risk of this complication. The incidence and severity of low phosphorus is not significantly different for the different ADV-based treatment regimens.

[Clinical features and gene mutation profiles of patients with chronic hepatitis B and Gilbert's syndrome].

OBJECTIVE: To explore the clinical features and gene mutation profiles of patients with chronic hepatitis B (CHB) and Gilbert's syndrome. METHODS: Thirty-three patients with CHB and Gilbert's syndrome were enrolled in the study. Serum markers of liver function and histological features of disease-related liver injury were assessed by standard methods. Gene mutations were detected by PCR and direct DNA sequencing.Statistical analysis was carried out with the chi-square and t tests. RESULTS: Sequencing of the Gilbert syndrome-associated gene, UGT 1A 1, revealed mutations in the upstream promoter phenobarbital-responsive element module (PBREM) (-3279 mutation, 23 cases), in the promoter TATA box (a TA insertion mutation, 21 cases), and in the coding region of exon 1 (a GGA-AGA Gly71Arg mutation, 18 cases); there was no statistical difference found for any of the three mutations among this patient population (x2 =1.640, P more than 0.05). CONCLUSION: The traditional methods of diagnosis for patients with CHB and Gilbert's syndrome remain a technical challenge in the clinic, and gene detection may represent a more favorable method for diagnosing this patient population.