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Xie H.,Nanjing Medical University | Xia K.,The Affiliated Jiangyin Hospital of Southeast University Medical College | Xia K.,Nanjing Medical University | Rong H.,Nanjing Medical University | And 2 more authors.
Breast | Year: 2013

8-hydroxy-2'-deoxyguanine (8-OHdG), a typical product of oxidative stress-induced DNA damage, can cause a G-T transversion during DNA replication if it is not removed. Human 8-oxoguanine glycosylase 1 ( hOGG1), a key DNA repair gene, recognizes and excises 8-OHdG from damaged DNA accurately; however, a c.977C>G (Ser326Cys) polymorphism in hOGG1 can inhibit the gene's ability to remove 8-OHdG. The aim of present study was to investigate the association between the c.977C>G polymorphism in hOGG1 and the risk of breast cancer in Chinese Han women. We used high-resolution melting and sequencing to analyze the genotypes of 630 patients with sporadic breast cancer patients and 777 healthy controls. We also performed risk-stratified subgroup analyses to determine the association between the c.977C>G polymorphism and other characteristics of breast cancer subgroups. Breast cancer patients and healthy controls did not have significantly different of c.977C/G genotypes (odds ratio [OR]=1.10, 95% confidence interval [CI]=0.82-1.49, p=0.57) and c.977G/G genotypes (OR=1.34, 95% CI=0.97-1.84, p=0.09). However, the c.977G/G genotype was especially prevalent in breast cancer patients who were younger than 55 years (OR=1.58, 95% CI=1.05-2.39, p=0.04), were premenopausal status (OR=1.87, 95% CI=1.14-3.06, p=0.02), had triple-negative disease (OR=2.14, 95% CI=1.06-4.29, p=0.04), or p53-positive disease (OR=1.56, 95% CI=1.14-2.12, p=0.005). These findings suggest that the c.977C>G polymorphism in hOGG1 is associated with an increased risk of breast cancer in Chinese Han women who are younger than 55 years, premenopausal, triple-negative, or p53-positive subgroups. © 2013 Elsevier Ltd. Source


Cui L.,Soochow University of China | Zhou H.,Soochow University of China | Zhao H.,The Affiliated Jiangyin Hospital of Southeast University Medical College | Zhou Y.,Soochow University of China | And 11 more authors.
BMC Cancer | Year: 2012

Background: A growing body of evidence suggests that microRNAs (miRNAs) play an important role in cancer diagnosis and therapy. MicroRNA-99a (miR-99a), a potential tumor suppressor, is downregulated in several human malignancies. The expression and function of miR-99a, however, have not been investigated in human renal cell carcinoma (RCC) so far. We therefore examined the expression of miR-99a in RCC cell lines and tissues, and assessed the impact of miR-99a on the tumorigenesis of RCC.Methods: MiR-99a levels in 40 pairs of RCC and matched adjacent non-tumor tissues were assessed by real-time quantitative Reverse Transcription PCR (qRT-PCR). The RCC cell lines 786-O and OS-RC-2 were transfected with miR-99a mimics to restore the expression of miR-99a. The effects of miR-99a were then assessed by cell proliferation, cell cycle, transwell, and colony formation assay. A murine xenograft model of RCC was used to confirm the effect of miR-99a on tumorigenicity in vivo. Potential target genes were identified by western blotting and luciferase reporter assay.Results: We found that miR-99a was remarkably downregulated in RCC and low expression level of miR-99a was correlated with poor survival of RCC patients. Restoration of miR-99a dramatically suppressed RCC cells growth, clonability, migration and invasion as well as induced G1-phase cell cycle arrest in vitro. Moreover, intratumoral delivery of miR-99a could inhibit tumor growth in murine xenograft models of human RCC. In addition, we also fond that mammalian target of rapamycin (mTOR) was a direct target of miR-99a in RCC cells. Furthermore, siRNA-mediated knockdown of mTOR partially phenocopied the effect of miR-99a overexpression, suggesting that the tumor suppressive role of miR-99a may be mediated primarily through mTOR regulation.Conclusions: Collectively, these results demonstrate for the first time, to our knowledge, that deregulation of miR-99a is involved in the etiology of RCC partially via direct targeting mTOR pathway, which suggests that miR-99a may offer an attractive new target for diagnostic and therapeutic intervention in RCC. © 2012 Cui et al.; licensee BioMed Central Ltd. Source


Yu G.P.,The Affiliated Jiangyin Hospital of Southeast University Medical College
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2011

The phosphatidylethanolamine-binding protein 4 (PEBP4) is a member of the PEBP family. It not only plays a role in the inhibition of the MAPK signaling pathway but also is involved in the inhibition of the JNK pathway that promotes the activation of AKT. Recent research has also shown that overexpression of PEBP4 was related to the development, invasion, and metastasis of a variety of tumors. This study aimed to investigate the correlation between PEBP4 protein expression in lung squamous cell carcinoma tissue and the clinical pathology of lung squamous cell carcinoma. Immunohistochemistry was used to detect PEBP4 expression in lung squamous cell carcinoma tissue and adjacent normal tissue from 61 patients. Western blotting was used to detect changes in the expression of PEBP4 protein between lung squamous cell carcinoma tissue and adjacent normal tissues. The correlation of PEBP4 expression and the occurrence, development, and clinical pathology of lung squamous cell carcinoma was analyzed. Of 61 patients, four patients were PEBP4 negative (-; 6.6%) and 57 patients were positive (+ to +++; 93.4%). Of those positive for PEBP4 expression, 7 patients were weakly positive (+; 11.5%), 21 patients were positive (++; 34.4%), and 29 patients were strongly positive (+++; 47.5%). PEBP4 protein was more highly expressed in lung squamous cell carcinoma tissue than in the adjacent normal lung tissue (p < 0.05). In PEBP4-positive patients, PEBP4 protein expression was significantly greater in those with lymph node metastases than in those without (p < 0.05). PEBP4 expression was significantly lower in patients at early (I and II) stages than in patients at advanced (III and IV) stages (p < 0.05). In less differentiated lung squamous cell carcinomas, PEBP4 protein expression was greater (p < 0.05); however, this was unrelated to the gender, age, or tumor size of the patient (p > 0.05). PEBP4 protein overexpression was associated with the occurrence, invasion, and metastasis of lung squamous cell carcinoma. Source


Zhuang Y.,Tongji University | Yin Q.,The Affiliated Jiangyin Hospital of Southeast University Medical College
Cell Biochemistry and Biophysics | Year: 2013

Changes in the composition and assembly of extracellular matrix (ECM) are the most prominent structure abnormalities of the vascular system encountered in early diabetes. Hyaluronan (HA) is a key biologically active element of ECM that plays a crucial role in vascular remodelling in atherosclerosis and restenosis following percutaneous coronary intervention. Hyperglycaemia led to significant increase in HA secretion by vascular smooth muscle cells. Hyperglycaemia also strongly induced HA synthase mRNA levels, notably HAS1-HAS3 mRNA. Remarkably, peroxisome proliferator-activated receptor (PPAR-γ) agonists pioglitazone (Pio) and rosiglitazone (Rosi), a class of anti-diabetic drugs, attenuated hyperglycaemia-induced HA secretion and reduced HAS2 mRNA expression. In vitro experiment with siRNA specific to PPAR-γ demonstrated that the attenuation of hyperglycaemia-induced HA secretion by Pio and Rosi was independent of PPAR-γ activity. Furthermore, hyperglycaemia-induced increase in HA secretion and HAS2 mRNA expression involved protein kinase Cβ2 (PKCβ2) activation, while Pio and Rosi exerted their attenuating effect on HA secretion by inhibiting PKCβ2. © 2013 Springer Science+Business Media New York. Source


Yin J.,Nanjing University | Zhao Z.,The Affiliated Jiangyin Hospital of Southeast University Medical College | Li Y.,Nanjing University | Wang J.,Nanjing University | And 5 more authors.
World Journal of Emergency Surgery | Year: 2014

Introduction: The optimal transfusion protocol remains unknown in the trauma setting. This retrospective cohort study aimed to determine if goal-directed transfusion protocol based on standard thrombelastography (TEG) is feasible and beneficial in patients with abdominal trauma.Methods: Sixty adult patients with abdominal trauma who received 2 or more units of red blood cell transfusion within 24 hours of admission were studied. Patients managed with goal-directed transfusion protocol via TEG (goal-directed group) were compared to patients admitted before utilization of the protocol (control group).Results: There were 29 patients in the goal-directed group and 31 in the control group. Baseline parameters were similar except for higher admission systolic blood pressure in the goal-directed group than the control group (121.8 ± 23.1 mmHg vs 102.7 ± 26.5 mmHg, p < 0.01). At 24 h, patients in the goal-directed group had shorter aPTT compared to patients in the control group (39.2 ± 16.3 s vs 58.6 ± 36.6 s, p = 0.044). Administration of total blood products at 24 h appeared to be fewer in the goal-directed group than the control group (10.2 [7.0-43.1]U vs 14.8 [8.3-37.6]U, p = 0.28), but this was not statistically significant. Subgroup analysis including patients with ISS ≥16 showed that patients in the goal-directed group had significantly fewer consumption of total blood products than patients in the control group (7[6.1, 47.0]U vs 37.6[14.5, 89.9]U, p = 0.015). No differences were found in mortality at 28d, length of stay in intensive care unit and hospital between the two groups.Conclusions: Goal-directed transfusion protocol via standard TEG was achievable in patients with abdominal trauma. The novel protocol, compared to conventional transfusion management, has the potential to decrease blood product utilization and prevent exacerbation of coagulation function. © 2014 Yin et al.; licensee BioMed Central Ltd. Source

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