First Peoples Hospital of Yueyang

Yueyang, China

First Peoples Hospital of Yueyang

Yueyang, China
SEARCH FILTERS
Time filter
Source Type

Shen E.,First Peoples Hospital of Yueyang | Liu C.,Shanghai University | Wei L.,401 Hospital of PLA | Hu J.,First Peoples Hospital of Yueyang | And 3 more authors.
Tumor Biology | Year: 2014

Background: Published data regarding the association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility remained controversial. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. Materials and methods: We systematically searched PubMed, Embase, and Web of Science with a time limit of August 19, 2013. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility using random-effects model. Results: A total of eight case-control studies including 2,597 cases and 3,063 controls were included for analysis. Overall, no significant associations were found between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility for GG vs TT (OR = 1.00, 95 % CI = 0.73-1.36, p = 0.00 for heterogeneity), TG vs TT (OR = 1.17, 95 % CI = 0.88-1.55, p = 0.00 for heterogeneity), the dominant model GG + TG vs TT (OR = 1.21, 95 % CI = 0.91-1.60, p = 0.00 for heterogeneity) nor the recessive model GG vs TG + TT(OR = 0.95, 95 % CI = 0.75-1.20, p = 0.02 for heterogeneity). In subgroup analysis, no significant associations were found in the Asian or Caucasian populations. Conclusion: This meta-analysis suggested that the APE1 Asp148Glu polymorphism was not associated with colorectal cancer susceptibility among Asians or Caucasians. © 2013 International Society of Oncology and BioMarkers (ISOBM).


Hu J.,First Peoples Hospital of Yueyang | Liu C.,Shanghai University | Yin Q.,First Peoples Hospital of Yueyang | Ying M.,Shanghai University | And 4 more authors.
Molecular Genetics and Genomics | Year: 2014

To date, epidemiological studies have assessed the association between CYP1A2-164 A/C polymorphism and colorectal cancer susceptibility. However, the results of these studies remained controversial. We aimed to examine the associations by conducting a meta-analysis of case-control studies. A total of 11 studies including 5,093 cases and 5,941 controls evaluated the association between the CYP1A2-164 A/C polymorphism and colorectal cancer susceptibility. No significantly associations were found in all genetic models (CC vs. AA: OR = 1.14, 95 % CI = 0.93-1.40; AC vs. AA: OR = 1.05, 95 % CI = 0.91-1.20; dominant model: OR = 1.08, 95 % CI = 0.95-1.24; recessive model: OR = 1.10, 95 % CI = 0.95-1.28). In the subgroup analysis by ethnicity or source of controls, there were still no significant associations detected in all genetic models. This meta-analysis suggested the CYP1A2-164 A/C polymorphism was not a risk factor for increasing colorectal cancer, further large and well-designed studies are needed to confirm these conclusions. © 2014 Springer-Verlag.


Liu C.,Shanghai University | Yin Q.,First Peoples Hospital of Yueyang | Hu J.,First Peoples Hospital of Yueyang | Weng J.,First Peoples Hospital of Yueyang | Wang Y.,Shanghai University
Tumor Biology | Year: 2014

Published data regarding the association between XPG Asp1104His polymorphism and bladder cancer risk remained controversial. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase, and Web of Science with a time limit of June 22, 2013. Summary odds ratios (ORs) with 95% CIs were used to assess the strength of the association between XPG Asp1104His polymorphism and bladder cancer risk using random effects model. A total of eight case-control studies including 2,613 cases and 2,934 controls were included for analysis. Overall, no significant association was found between XPG Asp1104His polymorphism and bladder cancer susceptibility for CC vs. GG (OR=1.12, 95% CI=0.74-1.69), GC vs. GG (OR=1.12, 95% CI=0.86-1.46), the dominant model CC + GC vs. GG (OR=1.08, 95% CI=0.85-1.38), and the recessive model CC vs. GC + GG (OR=0.92, 95% CI=0.66-1.29). In the subgroup analysis, no significant associations were found in either Asian or non-Asian population. This meta-analysis suggested that XPG Asp1104His polymorphism was not associated with bladder cancer risk. © International Society of Oncology and BioMarkers (ISOBM) 2013.


Liu C.,Shanghai University | Yin Q.,First Peoples Hospital of Yueyang | Li L.,Yueyang Second Peoples Hospital | Jiao G.,Peking University | And 2 more authors.
Critical Reviews in Eukaryotic Gene Expression | Year: 2013

The XRCC1 Arg194Trp and Arg280His polymorphisms were likely to be involved with the development of bladder cancer. However, there had been inconsistent reports of association. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship. We systematically searched PubMed, Embase, and Web of Science for relevant articles with a time limit of April 25, 2013. Summary odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association between the two polymorphisms and bladder cancer susceptibility using a random-effects model. This meta-analysis including 14 case-control studies evaluated the associations between the two XRCC1 polymorphisms and bladder cancer susceptibility. Overall, for Arg194Trp, significant associations were found in TT versus CC (OR = 1.78, 95% CI = 1.12-2.82) and the recessive model (OR = 1.71, 95% CI = 1.11-2.65); for Arg280His, significant associations were also found in AG versus GG (OR = 1.63, 95% CI =1.24-2.13) and the dominant model (OR =1.39, 95% CI = 1.07-1.82). When stratified by ethnicity, in Asian population, significant associations were found for Arg194Trp polymorphism in TT versus CC (OR = 2.99, 95% CI = 1.48-6.06), the dominant model (OR = 1.33, 95% CI = 1.03-1.72) and the recessive model (OR = 2.72, 95% CI = 1.36-5.45), and for Arg280His in GA versus GG (OR = 2.13, 95% CI = 1.63-2.97), but no significant associations were found in no-Asian population. This meta-analysis suggested that XRCC1 Arg194Trp and Arg280His polymorphisms were risk factors for increasing bladder cancer in Asian population. © 2013 Begell House, Inc.


Liu C.,Shanghai University | Yin Q.,First Peoples Hospital of Yueyang | Hu J.,First Peoples Hospital of Yueyang | Li L.,Yueyang Second Peoples Hospital | And 2 more authors.
Tumor Biology | Year: 2013

Published data regarding the association between the XPC polymorphisms and lung cancer susceptibility remained controversial. This meta-analysis was performed to draw a precise estimation of the relationship. We systematically searched PubMed, Embase, Elsevier, and Web of Science with a time limit of September 10, 2012. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of association between these polymorphisms and lung cancer susceptibility using random-effects model. This meta-analysis including 13 case-control studies evaluated the associations between three commonly XPC polymorphisms (Lys939Gln, Ala499Val, and PAT-/+) and lung cancer susceptibility. No significant associations were found between the three XPC polymorphisms and lung cancer susceptibility (for Lys939Gln polymorphism: CC vs AA, OR = 1.191, p = 0.033; AC vs AA, OR = 0.992, p = 0.762, the dominant model, OR = 1.028, p = 0.521; the recessive model, OR = 1.205, p = 0.022). For Ala499Val polymorphism: TT vs CC, OR = 1.195, p = 0.071; TC vs CC, OR = 1.146, p = 0.133; the dominant model, OR = 1.161, p = 0.086; the recessive model, OR = 1.123, p = 0.156. For PAT-/+ polymorphism: +/+ vs -/-, OR = 1.094, p = 0.539; +/- vs -/-, OR = 0.925, p = 0.313; the dominant model, OR = 0.969, p = 0.725; the recessive model, OR = 1.135, p = 0.290. p = 0.004 for Bonferroni testing). Significant associations were also not found in the subgroup analysis for the three XPC polymorphisms. This meta-analysis suggested that the three XPC polymorphisms might not be risk factors for developing lung cancer. © 2013 International Society of Oncology and BioMarkers (ISOBM).


Yang D.,First Peoples Hospital of Yueyang | Liu C.,Second Military Medical University | Shi J.,Shanghai JiaoTong University | Wang N.,Second Military Medical University | And 3 more authors.
Gene | Year: 2014

Genetic variations in DNA repair genes are thought to modify DNA repair capacity and may to be related to cancer susceptibility. However, epidemiological study results have been inconsistent. In this meta-analysis, we assessed 24 case-control studies of association between the X-ray repair cross complementing group 1 (XRCC1) Arg399Gln polymorphism and bladder cancer susceptibility in the general population and in Asian and non-Asian subgroups. A moderately significant association with bladder cancer risk was found for AG vs GG (OR. = 1.110, 95% CI. = 1.018-1.210). No significant associations with bladder cancer risk were found for AA vs GG (OR. = 0.942, 95% CI. = 0.823-1.077), the dominant model AA/AG vs GG (OR. = 1.075, 95% CI. = 0.990-1.167) and the recessive model AA vs AG/GG(OR. = 0.890, 95% CI. = 0.788-1.005). In subgroup analysis, a moderately significant association was also found for AG vs GG (OR. = 1.091, 95% CI. = 1.008-1.180) in non-Asian subgroup. The analysis suggests that the XRCC1 Arg399Gln polymorphism might be a moderate risk factor for bladder cancer, especially in non-Asian population. © 2013 Elsevier B.V.


Liu A.,University of South China | Liu A.,Changsha Central Hospital | Huang W.,University of South China | Zeng G.,University of South China | And 5 more authors.
Molecular Medicine Reports | Year: 2014

Nasopharyngeal carcinoma (NPC) has a highly increased incidence rate (20/100,000) in Southern regions of China, while being rare in the rest of the world. NPC is a malignant type of cancer due to its high occurrence rate of metastasis; however, biomarkers for effective diagnosis and treatment are yet to be identified. Annexin A1 is a glucocorticoid-regulated member of a large superfamily of calcium and phospholipid-binding proteins and has been shown to have important roles in tumor development and progression, and was demonstrated to be a prognostic biomarker for head and neck cancer types. A previous study by our group showed that Annexin A1 was decreased in NPC tissue as compared with normal adjacent tissue. To investigate whether Annexin A1 is a potential biomarker for NPC, the present study assessed the effect of the Annexin A1 on the biological behavior (i.e., invasion and metastasis) of the highly metastatic NPC cell line 5-8F and the non-metastatic NPC cell line 6-10B. The expression levels of Annexin A1 in the above two cell lines were determined by western blot analysis. Next, the recombinant plasmid pEGFP-C1-Annexin A1 and the small interfering (si)RNA plasmid pRNAT-U6.1-Annexin A1 were used and stably transfected into 5-8F and 6-10B cells, respectively. These established recombinant cell lines were then used to study the up- and downregulation of Annexin A1, respectively. The correlation of Annexin A1 expression levels with the biological behavior of NPC cell lines was analyzed using a cell proliferation assay, flow cytometry, soft agar colony formation assay, as well as Transwell invasion and migration assays. The results demonstrated that upregulation of Annexin A1 suppressed the proliferation, invasion and migration of NPC cells, while downregulation of Annexin A1 promoted the proliferation, invasion and migration of NPC cells. These findings suggested that Annexin A1 may be a potential biomarker for the development and prognosis of NPC, and its dysregulation may have an important role in its underlying pathogenesis.


Wu Z.,Wenzhou University | Cai X.,First Peoples Hospital of Yueyang | Huang C.,First Peoples Hospital of Yueyang | Xu J.,First Peoples Hospital of Yueyang | Liu A.,First Peoples Hospital of Yueyang
Oncology Reports | Year: 2016

Angiogenesis is a key factor in the growth and dissemination of malignant diseases, including breast cancer, with significant implications for its clinical management. It is known that microRNAs (miRNAs) play important roles in regulating tumor properties in cancers. However, whether miR-497 contributes to breast cancer angiogenesis remains unknown. Our study demonstrated that miR-497 was significantly downregulated in breast cancer tissue samples and cell lines. Conditioned medium obtained from breast cancer cell line MCF-7, treated with miR-497 mimics, suppressed the proliferation and tube formation of human umbilical vein endothelial cells in vitro, in comparison with the untransfected cells or cells transfected with the control vector alone. Furthermore, western blot assay confirmed that the overexpression of miR-497 reduced VEGF and HIF-1α protein levels. In addition, stable transfection of miR-497 inhibited tumorigenicity and angiogenesis in vivo. Moreover, HIF-1α was also increased in the breast cancer cells under a hypoxic condition, while the ectopic expression of miR-497 partially restored its level. Taken together, our findings indicate that miR-497 is a potential target for the biological therapy of breast cancer. Moreover, miR-497 inhibited the growth of tumors and reduced angiogenesis in a nude mouse xenograft tumor model, which was probably caused by the downregulation of pro-angiogenic molecules, such as VEGF and HIF-1α.


Peng L.,Wenzhou Medical College | Peng L.,Affiliated Hospital of Hainan Medical College | Liu A.,First Peoples Hospital of Yueyang | Shen Y.,Wenzhou Medical College | And 11 more authors.
Oncology Reports | Year: 2013

Thymoquinone (TQ), the predominant bioactive constituent derived from the medicinal spice Nigella sativa (also known as black cumin), has been applied for medical purposes for more than 2,000 years. Recent studies reported that thymoquinone exhibited inhibitory effects on the cell proliferation of several cancer cell lines. This study was performed to investigate the antitumor and anti-angiogenic effects of thymoquinone on osteosarcoma in vitro and in vivo. Our results showed that thymoquinone induced a higher percentage of growth inhibition and apoptosis in the human osteosarcoma cell line SaOS-2 compared to that of control, and thymoquinone significantly blocked human umbilical vein endothelial cell (HUVEC) tube formation in a dose-dependent manner. To investigate the possible mechanisms involved in these events, we performed electrophoretic mobility shift assay (EMSA) and western blot analysis, and found that thymoquinone significantly downregulated NF-κB DNA-binding activity, XIAP, survivin and VEGF in SaOS-2 cells. Moreover, the expression of cleaved caspase-3 and Smac were upregulated in SaOS-2 cells after treatment with thymoquinone. In addition to these in vitro results, we also found that thymoquinone inhibits tumor angiogenesis and tumor growth through suppressing NF-κB and its regulated molecules. Collectively, our results demonstrate that thymoquinone effectively inhibits tumor growth and angiogenesis both in vitro and in vivo. Moreover, inhibition of NF-κB and downstream effector molecules is a possible underlying mechanism of the antitumor and anti-angiogenic activity of thymoquinone in osteosarcoma.


Lei M.,Central South University | Tang Z.,Central South University | Tang Z.,First Peoples Hospital of Yueyang
Journal of Central South University (Medical Sciences) | Year: 2010

Objective To evaluate the effect of intermittent high glucose on the apoptosis of human umbilical vein endothelial cells (HUVECs) and its mechanism. Methods Intermittent high glucose and constant high glucose were applied to HUVEC-12 for 7 days. Flow cytometer and fluorescent staining with Hoechst 33258 were used to detect apoptosis of HUVEC-12. The superoxide dismutase (SOD) activity and the content of malonaldehyde (MDA) in culture solution were detected with colorimetry, and the changes of p -JNK level were examined by Western blot. Results The apoptosis rate was obviously higher in the intermittent high glucose group than that in the constant high glucose group (P < 0.05). The SOD activity was significantly lower in the intermittent high glucose group (P < 0.05), but MDA level was higher than those of constant high glucose (P < 0.05). SP600125, the inhibitor of JNK, decreased the apoptosis rate induced by intermittent high glucose (P<0.05). Antioxidant (Vitamin C) inhibited the p-JNK, decreased the apoptosis rate (P<0.05). Conclusion Intermittent high glucose is easier to worsen the proapoptotic effects on HUVECs than that of constant high glucose, which may account for the increased oxidative stress, and then activates JNK signal transduction pathway.

Loading First Peoples Hospital of Yueyang collaborators
Loading First Peoples Hospital of Yueyang collaborators