Ganzhou Cancer Hospital

Ganzhou, China

Ganzhou Cancer Hospital

Ganzhou, China
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Li S.,Ganzhou Institute of Cancer Research | Zhang X.,Ganzhou Institute of Cancer Research | Li R.,Ganzhou Institute of Cancer Research | Liu L.,Ganzhou Institute of Cancer Research | And 3 more authors.
Chinese Journal of Clinical Oncology | Year: 2014

Objective: A study was conducted to determine the expression of acetyl-coa carboxylase product of phosphorylation (P-ACC) and an enzyme called cyclooxygenase 2 (COX-2) in non-small cell lung cancer (NSCLC) tissue, as well as the relationship and correlations between tumor size, lymph node metastasis, clinical stage, and pathological type. Methods: Sixty-two patients with NSCLC lung cancer tissues were included in the patient group, whereas 20 patients who underwent lobectomy for other reasons and had normal lung tissues were included in the control group. Immunohistochemical streptavidin peroxidase method was used to detect the expression of P-ACC and COX-2 in lung cancer and normal lung tissues. Results: The positive expressions of P-ACC and COX-2 in NSCLC lung cancer and normal lung tissues were significantly different (P<0.05). In NSCLC tissues, the positive expression of P-ACC was significantly associated with tumor size (P<0.05), but was not significantly associated with lymph node metastasis, clinical stage, and pathological type. We found no correlation between the positive expression of COX-2 and tumor size, lymph node metastasis, clinical stage and pathological type. Further analysis revealed that the positive expression of P-ACC and COX-2 in NSCLC was significantly and negatively correlated (r=-2.37, P=0.032). Conclusion: The positive expression of COX-2 in NSCLC greatly increased compared with that of P-ACC, and a significantly negative correlation was observed between them. We propose that the positive expression of P-ACC reduction may activate the positive expression of COX-2 and promote the occurrence, development, invasion, and metastasis of NSCLC.


Liu Y.,Nanchang University | Liu Y.,Ganzhou Cancer Hospital | Fu Y.-Q.,Nanchang University | Peng W.-J.,Nanchang University | And 6 more authors.
Journal of Cardiovascular Pharmacology | Year: 2016

Adhesion of monocytes to the vascular endothelium is crucial in atherosclerosis development. Connexins (Cxs) which form hemichannels or gap junctions, modulate monocyteendothelium interaction. We previously found that rutaecarpine, an active ingredient of the Chinese herbal medicine Evodia, reversed the altered Cx expression induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells, and consequently decreases the adhesive properties of endothelial cells to monocytes. This study further investigated the effect of rutaecarpine on Cx expression in monocytes exposed to ox-LDL. In cultured human monocytic cell line THP-1, ox-LDL rapidly reduced the level of atheroprotective Cx37 but enhanced that of atherogenic Cx43, thereby inhibiting adenosine triphosphate release through hemichannels. Pretreatment with rutaecarpine recovered the expression of Cx37 but inhibited the upregulation of Cx43 induced by ox-LDL, thereby improving adenosine triphosphate-dependent hemichannel activity and preventing monocyte adhesion. These effects of rutaecarpine were attenuated by capsazepine, an antagonist of transient receptor potential vanilloid subtype 1. The antiadhesive effects of rutaecarpine were also attenuated by hemichannel blocker 18a-GA. This study provides additional evidence that rutaecarpine can modulate Cx expression through transient receptor potential vanilloid subtype 1 activation in monocytes, which contributes to the antiadhesive properties of rutaecarpine. © 2016 Wolters Kluwer Health, Inc. All rights reserved.


Peng W.-J.,Nanchang University | Liu Y.,Ganzhou Cancer Hospital | Yu Y.-R.,Nanchang University | Fu Y.-Q.,Nanchang University | And 5 more authors.
European Journal of Pharmacology | Year: 2015

Abstract Gap junctions, which is formed by connexins, has been proved to play an important role in the atherogenesis development. Rutaecarpine was reported to inhibited monocyte migration, which indicates its potential for anti-atherosclerosis activity. This study evaluated the effect of rutaecarpine on endothelial dysfunction, and focused on the regulation of connexin expression in endothelial cells by rutaecarpine. Endothelia damage was induced by exposing HUVEC-12 to Ox-LDL (100 mg/l) for 24 h, which decreased the expression of protective proteins Cx37 and Cx40, but induced atherogenic Cx43 expression, in both mRNA and protein levels, concomitant with the impaired propidium iodide diffusion through the gap junctions. Pretreatment with rutaecarpine effectively recovered the expression of Cx37 and Cx40, but inhibited Cx43 expression, thereby improving gap junction communication and significantly prevented the endothelial dysfunction. Consequently, the cell viability and nitric oxide production were increased, lactate dehydrogenase production was decreased and monocyte adhesion was inhibited. These protective effects of rutaecarpine were remarkably attenuated by pretreatment with capsazepine, a competitive antagonist of transient receptor potential vanilloid subtype 1 (TRPV1). In summary, this study is the first to report that rutaecarpine prevents endothelial injury and gap junction dysfunction induced by Ox-LDL in vitro, which is related to regulation of connexin expression patterns via TRPV1 activation. These results suggest that rutaecarpine has the potential for use as an anti-atherosclerosis agent with a novel mechanism. © 2015 Elsevier B.V. All rights reserved.


PubMed | Nanchang University and Ganzhou Cancer Hospital
Type: | Journal: European journal of pharmacology | Year: 2015

Gap junctions, which is formed by connexins, has been proved to play an important role in the atherogenesis development. Rutaecarpine was reported to inhibited monocyte migration, which indicates its potential for anti-atherosclerosis activity. This study evaluated the effect of rutaecarpine on endothelial dysfunction, and focused on the regulation of connexin expression in endothelial cells by rutaecarpine. Endothelia damage was induced by exposing HUVEC-12 to Ox-LDL (100mg/l) for 24h, which decreased the expression of protective proteins Cx37 and Cx40, but induced atherogenic Cx43 expression, in both mRNA and protein levels, concomitant with the impaired propidium iodide diffusion through the gap junctions. Pretreatment with rutaecarpine effectively recovered the expression of Cx37 and Cx40, but inhibited Cx43 expression, thereby improving gap junction communication and significantly prevented the endothelial dysfunction. Consequently, the cell viability and nitric oxide production were increased, lactate dehydrogenase production was decreased and monocyte adhesion was inhibited. These protective effects of rutaecarpine were remarkably attenuated by pretreatment with capsazepine, a competitive antagonist of transient receptor potential vanilloid subtype 1 (TRPV1). In summary, this study is the first to report that rutaecarpine prevents endothelial injury and gap junction dysfunction induced by Ox-LDL in vitro, which is related to regulation of connexin expression patterns via TRPV1 activation. These results suggest that rutaecarpine has the potential for use as an anti-atherosclerosis agent with a novel mechanism.


Luo Z.,Southern Medical University | Luo Z.,Ganzhou Cancer Hospital | Zeng H.,Ganzhou Cancer Hospital | Ye Y.,Ganzhou Cancer Hospital | And 4 more authors.
Molecular Medicine Reports | Year: 2015

Breast cancer accounts for 22.9% of all types of cancer in females worldwide. Safflower polysaccharide (SPS) is an active fraction purified from safflower petals (Carthamus tinctorius L). The present study investigated the effects of safflower polysaccharide on the proliferation and metastasis of breast cancer cells. Cell viability was analyzed using an MTT assay following treatment of the MCF-7 cells with increasing concentrations of SPS. The results demonstrated that the SPS compound significantly inhibited the proliferation of the MCF-7 human breast cancer cell line and these inhibitory effects increased in a dose- and time-dependent manner. The half maximal inhibitory concentration (IC50) value of SPS on breast cancer cells, following treatment for 72 h, was detected using an MTT assay and was calculated as 0.12 mg/ml. The apoptotic rate was detected using flow cytometry in the MCF-7 human breast cancer cell line and the results revealed that SPS induced cell apoptosis. The apoptotic rate of the MCF-7 cells treated with SPS was significantly higher compared with that of the untreated cells and increased in a dose-dependent manner. The expression of B-cell lymphoma 2 (Bcl-2) was downregulated and the expression of Bcl-2-associated X protein was upregulated in the MCF-7 cells treated with SPS in a time-dependent manner. Additionally, the expression of matrix metalloproteinase-9 was significantly reduced and the expression of tissue inhibitor of metalloproteinase-1 was increased in the MCF-7 human breast cancer cell treated with SPS. These results demonstrated that SPS inhibited the metastasis of MCF-7 breast cancer cells and understanding the underlying mechanisms may provide novel strategies in breast cancer therapy.


PubMed | Ganzhou Cancer Hospital and Southern Medical University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

Breast cancer accounts for 22.9% of all types of cancer in females worldwide. Safflower polysaccharide (SPS) is an active fraction purified from safflower petals (Carthamus tinctorius L). The present study investigated the effects of safflower polysaccharide on the proliferation and metastasis of breast cancer cells. Cell viability was analyzed using an MTT assay following treatment of the MCF7 cells with increasing concentrations of SPS. The results demonstrated that the SPS compound significantly inhibited the proliferation of the MCF7 human breast cancer cell line and these inhibitory effects increased in a dose and timedependent manner. The half maximal inhibitory concentration (IC50) value of SPS on breast cancer cells, following treatment for 72h, was detected using an MTT assay and was calculated as 0.12mg/ml. The apoptotic rate was detected using flow cytometry in the MCF7human breast cancer cell line and the results revealed that SPS induced cell apoptosis. The apoptotic rate of the MCF7cells treated with SPS was significantly higher compared with that of the untreated cells and increased in a dosedependent manner. The expression of Bcell lymphoma2 (Bcl2)was downregulated and the expression of Bcl2associatedXprotein was upregulated in the MCF7cells treated with SPS in a timedependent manner. Additionally, the expression of matrix metalloproteinase9 was significantly reduced and the expression of tissue inhibitor of metalloproteinase1 was increased in the MCF7human breast cancer cell treated with SPS. These results demonstrated that SPS inhibited the metastasis of MCF7breast cancer cells and understanding the underlying mechanisms may provide novel strategies in breast cancer therapy.


Li S.-J.,Ganzhou Cancer Hospital | Zhang X.-M.,Ganzhou Cancer Hospital | Li R.,Ganzhou Cancer Hospital | Liu L.-B.,Ganzhou Cancer Hospital | And 3 more authors.
Chinese Journal of Cancer Prevention and Treatment | Year: 2014

OBJECTIVE: To explore the expression of acetyl-coa carboxylase product of phosphorylation (P-ACC) and nuclear factor kappaB (NF-κB) in non-small cell lung cancer (NSCLC) tissue and the relationship of the tumor size, lymph node metastasis, clinical stage and pathological type, and study the correlation of them. METHODS: 62 cases of NSCLC tissue were as a patient group. Twenty cases normal lung tissues as controls. Immunohistochemical SP method was used in detection of the expression of P-ACC and NF-κB in lung cancer and normal lung tissue. The immunohistochemical SP expression of P-ACC and NF-κB was investigated in 60 NSCLC lung cancer tissue and 20 lung normal tissue because of other reasons for lobectomy. RESULTS: P-ACC 80.0% (16/20) positive expression in normal lung tissue and 33.9% (21/62) positive expression in NSCLC tissues, the difference was significant (P=0.0001). NF-κB was 15% positive expression in normal lung tissue and 75.8%(47/62) positive expression in NSCLC tissues, the difference was significant (P<0.05). In NSCLC, the positive expression of P-ACC was associated with tumor size significantly (P=0.033), but it was no correlation between lymph node metastasis, clinical stage and pathological type. We also found that there was no correlation between the positive expression of NF-κB and tumor size, lymph node metastasis, clinical stage but there was significant correlation with pathological type (P=0.008). Further analysis revealed that the positive expression of P-ACC and NF-κB in NSCLC was significantly negative correlation (r=-0.409, P<0.001). CONCLUSION: The reduced positive expression of P-ACC may activate positive expression of NF-κ B, and promote the occurrence, development, invasion and metastasis of NSCLC.

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