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Wang G.-Q.,the First Affiliated Hospital of Xi an Jiaotong University | Zhao W.-H.,Shaanxi Province Tumor Hospital | Nan K.-J.,the First Affiliated Hospital of Xi an Jiaotong University
Biomarkers | Year: 2016

Background: Interleukin-27 (IL-27) has been recognized as a pleiotropic cytokine with both pro- and anti-inflammatory properties. Patients and methods: A case-control study was conducted to investigate the possible associations of IL-27 gene polymorphisms with susceptibility to cervical cancer and clinical outcome. Results: Our results suggested that the IL-27 2905T/G was significantly associated with a decreased risk of cervical cancer. Further analysis showed IL-27 2905T/G genotypes were associated with advanced tumor stages of cervical cancer patients. More interestingly, the IL-27 2905T/G genotypes were statistically significantly associated with the survival in cervical cancer patients. Conclusion: Our results showed that the IL-27 2905T/G genotypes were associated with decreased the susceptibility and development of cervical cancer in Chinese Han population. © 2016 Taylor & Francis.


PubMed | the First Affiliated Hospital of Xi an Jiaotong University and Shaanxi Province Tumor Hospital
Type: Journal Article | Journal: Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals | Year: 2016

Interleukin-27 (IL-27) has been recognized as a pleiotropic cytokine with both pro- and anti-inflammatory properties.A case-control study was conducted to investigate the possible associations of IL-27 gene polymorphisms with susceptibility to cervical cancer and clinical outcome.Our results suggested that the IL-27 2905T/G was significantly associated with a decreased risk of cervical cancer. Further analysis showed IL-27 2905T/G genotypes were associated with advanced tumor stages of cervical cancer patients. More interestingly, the IL-27 2905T/G genotypes were statistically significantly associated with the survival in cervical cancer patients.Our results showed that the IL-27 2905T/G genotypes were associated with decreased the susceptibility and development of cervical cancer in Chinese Han population.


PubMed | The Center Hospital of Xian, Shaanxi Province Tumor Hospital and Xi'an Jiaotong University
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

SET7/9 is a protein lysine methyltransferase that had been initially identified as a histone lysine methyltransferase which generates monomethylation at histone 3 lysine 4. Different functions were attributed to the protein methylation mediated by SET7/9. In this study, we found that the expression of SET7/9 declined in a majority of the human breast cancer tissues examined compared with normal tissues. Knockdown of SET7/9 promoted the proliferation, migration, and invasion of breast cancer cells. Knockdown of SET7/9 also increased the tumorigenicity of breast cancer cells in vivo. On the contrary, overexpression of SET7/9 in breast cancer cells inhibited these processes. Microarray analysis indicated that Gli-1 may play function as a downstream factor of SET7/9. Overexpression of SET7/9SET7/9 inhibits Gli-1 expression. While knockdown of SET7/9 promotes the expression of Gli-1. Gli-1 inhibited by cyclopamine blocked knockdown SET7/9-driven proliferation, migration, and invasion in breast cancer cell. Furthermore, Gli-1 expression in human breast cancer tissues is negatively correlated with SET7/9 expression. Together, these results helped to realize the antioncogene functions of SET7/9 in breast cancer cells and provided a novel direction to treat breast cancer.


Du N.,Xi'an Jiaotong University | Feng J.,Yan'an University | Hu L.-J.,Xi'an Jiaotong University | Sun X.,Xi'an Jiaotong University | And 4 more authors.
Oncology Reports | Year: 2012

Chronic stress and a high-fat diet are well-documented risk factors associated with the renin-angiotensin system in the development of breast cancer. The angiotensin II type 1 receptor (AT1R) is a novel component of the reninangiotensin system. Several recent studies have focused on the function of AT1R in cell proliferation during cancer development. Thus, we hypothesized that angiotensin II (Ang .) can promote proliferation of breast cancer via activated AT1R; the activation of AT1R may play an important role in promoting breast cancer growth, and AT1R blocker (ARB) may suppress the promotional effect on proliferation by antagonizing AT1R. The expression level of AT1R was found to be significantly upregulated in breast cancer cells by immunohistochemistry, but no correlation between AT1R expression and ER/PR/ Her-2 expression was observed. The AT1R(+)-MCF-7 cell line exhibited high expression of AT1R protein, and we generated the AT1R(-)-MCF-7 cell line using RNA interference. ARBs, and in particular irbesartan, effectively inhibited the effects of Ang II on cell proliferation, cell cycle development and downstream AT1R signaling events, including the activation of the Ras-Raf-MAPK pathway and the transcription factors NF-κB and CREB. Irbesartan also significantly altered p53, PCNA and cyclin D1 expression, which was also influenced by activated AT1R in AT1R(+)-MCF-7 cells. These results suggest that ARBs may be useful as a novel preventive and therapeutic strategy for treating breast cancer.


Huo X.,Xi'an Jiaotong University | Li S.,Shaanxi Province Tumor Hospital | Shi T.,Xi'an Jiaotong University | Suo A.,Xi'an Jiaotong University | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2015

The present study was to examine the effect of Tripartite motif 16 (TRIM16) on epithelial-mesenchymal transition (EMT) and metastasis in non-small cell lung cancer (NSCLC) cells, and its clinical significance in NSCLC. The correlation of TRIM16 expression and clinical features of NSCLC was analyzed in paraffin-embedded archived normal lung tissues and NSCLC tissues by immunohistochemical analysis. The effect of TRIM16 on EMT and metastasis was examined both in vitro and in vivo. The expression of TRIM16 was markedly decreased in NSCLC and correlated with tumor metastasis. Upregulation of TRIM16 significantly inhibited EMT and metastasis of NSCLC cells. In contrast, silencing TRIM16 expression significantly promoted the EMT and metastasis of NSCLC cells both in vitro and in vivo. Moreover, we demonstrated that downregulation of TRIM16 activated the sonic hedgehog pathway, and that inhibition of the sonic hedgehog pathway by cyclopamine abrogated the effect of TRIM16-downregulation induced EMT and metastasis on NSCLC cells. Our results suggest that TRIM16 is a potential pharmacologic target for the treatment of NSCLC and promotion TRIM16 expression might represent a novel strategy to NSCLC metastasis. © 2015 Elsevier Inc. All rights reserved.


Liao Z.J.,Shaanxi Province Tumor Hospital | Liao Z.J.,Xi'an Jiaotong University | Guo Y.H.,Shaanxi Province Tumor Hospital | Zhao Z.,Shaanxi Province Tumor Hospital | And 3 more authors.
International Journal of Oncology | Year: 2014

Recurrence and metastasis are responsible for the death of non-small cell lung cancer (NSCLC) patients. Circulating tumor cells (CTCs) in the metastatic pathway have proven to be essential. This pilot study evaluated the sensitivity of gemcitabine in micrometastasis and CTCs from NSCLC patients. EpCAM-positive CTCs were detected in forty patients with NSCLC at treatment initiation and disease evaluation time-points. EpCAM-positive CTCs were defined as EpCAM-positive and CD45-negative. Total RNA was isolated from EpCAM-enriched CTCs and cytokeratin levels were detected by PCR. The HGF/cMET pathway was evaluated in CTCs from patients with different treatments and in A549 cells. The EMT-related markers were analyzed by IHC. We further explored the predictive value of baseline CTCs in patients that were receiving different treatments. The median number of CTCs in NSCLC patients was 65 CTCs/ml more than in the healthy 23-fold (median, 5.2 CTCs/ml). The mean change in cell count was significantly different for patients with gemcitabine compared to patients with non-gemcitabine treatments (-86.28 vs. -15.23/ml; P<0.05). A significant decrease was noted in the expression of cytokeratin in the CTCs of the two groups (P<0.05). The HGF/cMET pathway was inactivated in CTCs and A549 cells treated with gemcitabine, and the cell migration and invasion abilities were inhibited by gemcitabine via the HGF/cMET pathway. Furthermore, the decreased cell migration and invasion abilities may also be involved in the inhibition of the epithelial-mesenchymal transition (EMT) by gemcitabine. At a median follow-up of 36 months, the CTC count was confirmed to be a robust prognostic marker in the NSCLC population (CTCs >151, median: 15.0 months and CTCs <151, median: 32.0 months). Additionally, the survival rate in the gemcitabine group (24 months) was better than in non-gemcitabine group (21 months), suggesting a therapeutic benefit for NSCLC patient survival with the common therapy plus gemcitabine. Gemcitabine treatment decreased EpCAM-positive CTCs in NSCLC patients and inhibited EMT by the HGF/cMET pathway.


PubMed | Shaanxi Province Tumor Hospital and Xi'an Jiaotong University
Type: Journal Article | Journal: Oncotarget | Year: 2015

Metastasis is the leading cause of death in breast cancer (BC) patients. However, until now, the mechanisms of BC metastasis remain elusive. Cullin3 is a highly conserved Cullin family member present in the genomes of all eukaryotes, which has been proposed as an oncogene in many types of tumors; however, its role and underlying mechanisms in BC remain unclear. Here we show that Cullin3 is elevated in BC and its expression level is positively correlated with metastasis. Overexpression of Cullin3 in BC cells increased proliferation, epithelial-mesenchymal transition, migration and invasion in vitro, and enhanced tumorigenic and metastatic capacities in vivo. In contrast, silencing Cullin3 in aggressive and invasive BC cells inhibited these processes. Mechanistically, we found Cullin3 exerts its function through promoting BRMS1 protein degradation, which was associated with EMT, migration and invasion. BRMS1 overexpression blocked Cullin3-driven EMT, and metastasis. Our results, for the first time, portray a pivotal role of Cullin3 in stimulating metastatic behaviors of BC cells. Targeting Cullin3 may thus be a useful strategy to impede BC cell invasion and metastasis.


PubMed | Shaanxi Province Tumor Hospital and Xi'an Jiaotong University
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2015

The present study was to examine the effect of Tripartite motif 16 (TRIM16) on epithelial-mesenchymal transition (EMT) and metastasis in non-small cell lung cancer (NSCLC) cells, and its clinical significance in NSCLC. The correlation of TRIM16 expression and clinical features of NSCLC was analyzed in paraffin-embedded archived normal lung tissues and NSCLC tissues by immunohistochemical analysis. The effect of TRIM16 on EMT and metastasis was examined both in vitro and in vivo. The expression of TRIM16 was markedly decreased in NSCLC and correlated with tumor metastasis. Upregulation of TRIM16 significantly inhibited EMT and metastasis of NSCLC cells. In contrast, silencing TRIM16 expression significantly promoted the EMT and metastasis of NSCLC cells both in vitro and in vivo. Moreover, we demonstrated that downregulation of TRIM16 activated the sonic hedgehog pathway, and that inhibition of the sonic hedgehog pathway by cyclopamine abrogated the effect of TRIM16-downregulation induced EMT and metastasis on NSCLC cells. Our results suggest that TRIM16 is a potential pharmacologic target for the treatment of NSCLC and promotion TRIM16 expression might represent a novel strategy to NSCLC metastasis.


PubMed | Shaanxi Province Tumor Hospital and PLA Fourth Military Medical University
Type: Journal Article | Journal: PloS one | Year: 2014

Irrational use of antimicrobial agents for preventing postoperative SSIs is a common phenomenon in China, which results in more bacterial resistance, higher hospital infection rates, extra costs of antimicrobial agents. The aim of the study is to evaluate the effect of Drug Rational Usage Guidelines System (DRUGS) on the surgeons prescription behavior of antimicrobial agents.10 common surgical operations which included 1543 cases (where 778 cases using paper-based guidelines and 765 cases using DRUGS) were selected and their demographic and clinical data were collected. The selected operations include thyroid resection, breast mass resection, myomectomy, etc. The evaluation criteria were antibiotic administrative categories, the time of initial dose, duration of administration, length of stay, the costs of antibiotics, SSIs and drug adverse reactions(ADR).The antimicrobial agents were mostly administrated within 0.5 h to 2 h before incision, 656 patients (85.75%) were intervened with DRUGS and 256 (32.90%) with paper-based guidelines according to the protocol. For the clean wounds incision, 547 patients (91.62%) were within 24 h of withdrawal antibiotics with using paper-based guidelines versus 91 (14.79%) with using DRUGS. A total of 19 kinds of antibiotics were used in the 1543 cases. The leading three on the list of frequency were piperacillin and sulbactam sodium, cefathiamidine and cefoperazone. While after the intervention, the list of frequency changed to cefazolin, cefathiamidine, cefoperazone. The average hospital stay was (7.004.31)d with paper-based guidelines and (2.541.57)d with DRUGS, respectively. The average cost of antibiotics was (3481.362584.46) with paper-based guidelines and (1693.391478.27) with DRUGS, respectively. However, there were no significant differences in the incidence of SSIs and ADR between two groups.In this study, the increased availability of antibiotic guidelines at the time of drug ordering, combined with DRUGS, was associated with an enhanced surgeon adherence to guidelines.


Guo X.-X.,Northwest University, China | Song Z.-J.,Shaanxi Province Tumor Hospital | Sun J.-J.,Northwest University, China | Song J.-F.,Northwest University, China
Biosensors and Bioelectronics | Year: 2011

Since the electrochemical oxidation peaks of both DNA and anti-tumor drug tamoxifen (TAM) overlapped with each other, the known electrochemical methods were limited in the study of the interactions between DNA and TAM. In this paper, zero current potentiometry, a new electrochemical method, was used to study the interaction of calf thymus dsDNA with TAM. The dsDNA was immobilized on the surface of carbon paste (dsDNA/CP). The dsDNA/CP connected in series between the clips of working and counter electrodes of a potentiostat and a reference electrode were immersed in aqueous solution containing TAM, the interaction of dsDNA with TAM produced a change in interfacial potential at the dsDNA/CP/solution interface. When linear sweep potential was applied to the dsDNA/CP and the corresponding I-E curve was recorded, interfacial potential offset applied potential partially, making the I-E curve displace along potential axis. Zero current potential where circuit current I was equal to zero in the I-E curve was measured to check the displacement of the I-E curve. Based on the displacement, the thermodynamic constants of the interaction between dsDNA and TAM were determined. The binding ratio of dsDNA with TAM was found to be 1:1 and the apparent binding constant was (6.85±0.20)×106M-1. As zero current potentiometry was independent of the changes in redox potential or current of both dsDNA and TAM themselves, the interaction was studied in their natural forms without damage. Moreover, TAM can be determined. The detection limit was 1.1×10-7M. © 2011 Elsevier B.V.

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