Objective : To investigate the effect of exposure to low concentrations of benzene on miR-155 and miR-223 expression in peripheral blood lymphocytes among workers with benzene exposure. Methods : A hundred male employees at a risk of exposure to benzene (the exposed group) were randomly sampled from two small metal products manufacturing enterprises and one medium-sized chemical raw material and chemical products manufacturing enterprise in Ningbo City, Zhejiang Province, and 60 age-matched male employees without benzene exposure were randomly selected as the unexposed group. Age, body mass index ( BMI ), smoking status, alcohol consumption, disease history, medication history and routine blood testing results of subjects were collected using a questionnaire survey. The 8-hour time weighted average concentration ( CTWA ) of benzene was measured in the workplace using thermal desorption gas chromatography, and the urine 8-hydroxy-2' deoxyguanosine ( 8-OHdG ) levels were determined using high-performance liquid-chromatography tandem mass spectrometry (HPLC-MS/MS). The miR-155 and miR-223 expression was quantified in peripheral blood lymphocytes using quantitative fluorescent reverse transcription-polymerase chain reaction assay, and the factors affecting miR-155 and miR-223 expression were identified using multivariable logistic regression analysis. Results : The subjects in the exposed group had a mean age of ( 31.17±7.30 ) years, and were exposed to low concentrations of benzene ( CTWA, 0.05 to 0.30 mg/m3 ) , while the subjects in the unexposed group had a mean age of ( 32.52±6.15 ) years. There were no significant differences between the exposed and unexposed groups in terms of age, BMI, proportion of smokers or proportion of alcohol consumers ( P>0.05 ). There was no significant difference in the median relative miR-155 expression between the exposed and unexposed groups ( 0.953 vs. 1.293, P>0.05 ), and lower median relative miR-223 expression was quantified in the exposed group than in the unexposed group ( 0.540 vs. 1.433, P<0.05 ). Multivariable logistic regression analysis revealed that down-regulation of miR-223 expression correlated with exposure to benzene ( OR=2.719, 95%CI: 1.308-5.651 ). Conclusion Down-regulation of miR-223 expression may be associated with exposure to low concentrations of benzene.

Objective: To explore the action mechanism of miR-139-5p inhibiting proliferation and invasion of epithelial ovarian cancer (EOC) cells by targetedly regulatingNotch1.Methods: A total of 24 pairs of EOC tissues and its corresponding para-cancerous tissues from patients, who underwent surgical resection in the DepartmentofGynecology,Nanyang Central Hospital of Henan Province, were collected for this study; in addition, human ovarian cancer cell lines (SKOV3, ES2, HEY-T30) and human ovarian epithelial cell line IOSE80 were also collected. Real-time quantitative PCR (qPCR) was applied to detectmRNAexpressionofmiR-139-5pandNotch1 in EOC tissues and cell lines. The miR-139-5p over-expression vector and recombinant plasmid pLV-Notch1 were transfected into SKOV3 cells. Blank control group (Ctrl group) and negative control group (NC group) were set up. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-139-5p and Notch1 3'-UTR. CCK-8, Transwell and Scratch healing experiments were applied to detect cell proliferationinvasionandmigration, respectively. Western blotting was applied to detect expressions of proliferation and migration related proteins in cells. Results: Compared with para-cancerous tissues and IOSE80 cells, the expression of miR-139-5p was significantly decreased in EOC tissues and cell lines, while the expression of Notch1 mRNA was significantly increased (all P<0.01). The results of Dual luciferase reporter showed that Notch1 was the downstream target gene of miR-139-5p. Compared with NC group, cell proliferation, invasion and migration ability, expression levels of Notch1, NICD, Cyclin D1, Cyclin A1, Snail1, β-catenin and N-cadherin were all significantly decreased on 3 d in miR-139-5p mimic group (all P<0.01), while expression of E-cadherin was significantly increased (P<0.01); meanwhile, over-expression of Notch1 could reverse the inhibitory effect of miR-1395p on proliferation, invasion and migration of SKOV3 cells. Conclusion: miR-139-5p can targetedly regulate Notch1 to inhibit proliferation, invasion and migration of EOC cells, which may be related to its down-regulation of NICD, Cyclin D1, Cyclin A1, Snail1, βcatenin and N-cadherin, and up-regulation of E-cadherin.