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Wang C.,Harbin Medical University | Li P.,Harbin Medical University | Lian A.,Harbin Medical University | Sun B.,Harbin Medical University | And 14 more authors.
Cancer Biology and Therapy | Year: 2014

Many recent studies have focused on the connection between the composition of specific volatile organic compounds (VOCs) in exhaled breath and various forms of cancer. However, the composition of exhaled breath is affected by many factors, such as lung disease, smoking, and diet. VOCs are released into the bloodstream before they are exhaled; therefore, the analysis of VOCs in blood will provide more accurate results than the analysis of VOCs in exhaled breath. Blood were collected from 16 colorectal cancer patients and 20 healthy controls, then solid phase microextraction-chromatography- mass spectrometry (SPME-GC-MS) was used to analysis the exhaled volatile organic compounds (VOCs). The statistical methods principal component analysis (PCA) and partial least-squares discriminant analysis (PLSDA) were performed to deal with the final dates. Three metabolic biomarkers were found at significantly lower levels in the group of CRC patients than in the normal control group (P < 0.01): phenyl methylcarbamate, ethylhexanol, and 6-t-butyl-2,2,9,9-tetramethyl-3,5- decadien-7-yne. In addition, significantly higher levels of 1,1,4,4-tetramethyl- 2,5-dimethylene-cyclohexane were found in the group of CRC patients than in the normal control group (P < 0.05). Compared with healthy individuals, patients with colorectal adenocarcinoma exhibited a distinct blood metabolic profile with respect to VOCs. The analysis of blood VOCs appears to have potential clinical applications for CRC screening. © 2014 Landes Bioscience. Source


Li A.,Heilongjiang Key Laboratory of Immunity and Infection | Qian J.,Heilongjiang Key Laboratory of Immunity and Infection | He J.,Heilongjiang Key Laboratory of Immunity and Infection | Zhang Q.,Heilongjiang Key Laboratory of Immunity and Infection | And 6 more authors.
Molecular Medicine Reports | Year: 2013

Type I interferon (IFN) is believed to play significant roles in limiting tumor growth. It has been revealed that the induction of endogenous IFN expression is one of the key mechanisms for successful IFN therapy. However, recent studies have shown that the efficacy of type I IFN therapy has limitations in the clinical treatment of certain tumors, including hepatocellular carcinoma (HCC). It has been revealed that the expression of miR-122 is significantly decreased in HCC and that restoration of miR-122 expression may improve the prognosis of this condition. Previous studies also showed that patients with low miR-122 levels in the liver responded poorly to the IFN therapy. We previously identified that the IFN expression was reduced when miR-122 was suppressed in human oligodendrocytes. Based on these studies, it was hypothesized that the expression of miR-122 may modulate the endogenous IFN expression and subsequently affect the treatment outcome of IFN therapy for HCC. The results of the present study showed that miR-122 abundant Huh7 cells responded more significantly than miR-122 deficient HepG2 cells when treated with exogenous IFN. Upregulation of miR-122 significantly increased the ability of exogenous IFN induced IFN expression, while downregulation of miR-122 decreased this ability. These data indicate that a high level of miR-122 expression may promote the expression of type I IFN induced by exogenous IFNs and further contribute to IFN therapy for HCC. Copyright © 2013 Spandidos Publications Ltd. Source


Song W.,Heilongjiang Key Laboratory of Immunity and Infection | Song W.,Harbin Medical University | Kao W.,Key Laboratory of Pathogenic Biology | Kao W.,Harbin Medical University | And 10 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

The expression of type I interferon (IFN) is one of the most potent innate defences against viral infection in higher vertebrates. Borna disease virus (BDV) establishes persistent, noncytolytic infections in animals and in cultured cells. Early studies have shown that the BDV phosphoprotein can inhibit the activation of type I IFN through the TBK1-IRF3 pathway. The function of the BDV nucleoprotein in the inhibition of IFN activity is not yet clear. In this study, we demonstrated IRF7 activation and increased IFN-α/β expression in a BDV-persistently infected human oligodendroglia cell line following RNA interference-mediated BDV nucleoprotein silencing. Furthermore, we showed that BDV nucleoprotein prevented the nuclear localisation of IRF7 and inhibited endogenous IFN induction by poly(I:C), coxsackie virus B3 and IFN-β. Our findings provide evidence for a previously undescribed mechanism by which the BDV nucleoprotein inhibits type I IFN expression by interfering with the IRF7 pathway. © 2013 Elsevier Inc. Source


He J.,Harbin Medical University | He J.,CAS Institute of Biophysics | Ji Y.,Harbin Medical University | Zhang Q.,Heilongjiang Key Laboratory of Immunity and Infection | And 15 more authors.
PLoS ONE | Year: 2014

Human Papillomavirus (HPV) 16 infection is considered as one of the significant causes of human cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several tumor development, while the effects of miR-122 on HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR- 122 function showed that miR-122 could directly bind with HPV16 E6 mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (STAT1) protein indicated that miR-122 might enhance type I interferon in cervical carcinoma cells, which explained the significant reduction of HPV16 E7 and E6∗I mRNA expression. This might be due to the binding between miR-122 and suppressor of cytokine signaling 1 (SOCS1) mRNA, which is the suppressor of interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1 mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6 mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting HPV infection. © 2014 He et al. Source


Hu Y.L.,Harbin Medical University | Hu Y.L.,Heilongjiang Key Laboratory of Immunity and Infection | Li H.,Harbin Medical University | Li H.,Heilongjiang Key Laboratory of Immunity and Infection | And 15 more authors.
Lupus | Year: 2013

Plasma gelsolin, the extracellular gelsolin isoform, circulates in the blood of healthy individuals at a concentration of 200 ± 50 mg/l and plays important roles in the extracellular actin-scavenging system during tissue damage. Decreased plasma gelsolin levels have been observed in many inflammatory diseases. In the present study, the variation and potential clinical application of plasma gelsolin levels in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) were analysed. Plasma samples and clinical data were collected from informed and consenting participants: 47 SLE patients, 60 RA patients and 50 age- and gender-matched healthy individuals. Semiquantitative western blotting was used for measuring plasma gelsolin levels. The plasma gelsolin levels in patients with SLE and RA were significantly decreased compared with healthy controls (145.3 ± 40.4 versus 182.7 ± 38.3 mg/l and 100.8 ± 36 versus 182.7 ± 38.3 mg/l, p < 0.001), and plasma gelsolin levels were especially lower in RA than in SLE patients (100.8 ± 36 versus 145.3 ± 40.4 mg/L, p < 0.001). An analysis of the clinical data showed a significant negative correlation between plasma gelsolin levels and SLE Disease Activity Index (SLEDAI) scores (r = 0.659, p < 0.001) but no correlation between plasma gelsolin levels and RA disease activity score 28 (DAS28) (r = 0.076, p = 0.569). Different clinical characteristics were also observed in SLE and RA patients with normal and decreased plasma gelsolin levels.This study found significantly lower plasma gelsolin levels in patients with SLE and RA compared with healthy controls and documented a significant negative correlation between plasma gelsolin levels and SLEDAI, which suggested the potential clinical application of plasma gelsolin in SLE diagnosis and disease activity evaluation. The different clinical characteristics in SLE and RA patients with normal and decreased plasma gelsolin levels indicate differences in the basis of the diseases. © 2013 The Author(s). Source

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