Publications (12)30.58 Total impact
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Article: Neurotransmitter substance P mediates pancreatic cancer perineural invasion via NK-1R in cancer cells.
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ABSTRACT: Pancreatic cancer significantly affects the quality of life due to the severe abdominal pain. However, the underlying mechanism is not clear. This study aimed to determine the relationship between SP and pancreatic cancer perineural invasion (PNI) as well as mechanism of SP mediating pancreatic cancer PNI which cause pain in patients with pancreatic cancer. Human pancreatic cancer cells and newborn dorsal root ganglions (DRGs) were used to determine the expression of SP or NK-1R in pancreatic cancer cells and DRGs cells by QT-PCR and Western blotting. The effects of SP on pancreatic cancer cell proliferation and invasion were analyzed using MTT assay and Transwell matrigel invasion assay, respectively. Alterations in the neurotropism of pancreatic cancer cells were assessed by co-culture system which mimics the interaction of tumor/neuron in vivo. SP is not only widely distributed in the neurite outgrowth from newborn DRGs but also expressed in MIA PaCa-2 and BxPC-3 cells. NK-1R is found to be overexpressed in the pancreatic cancer cell lines examined. SP induces cancer cell proliferation and invasion as well as the expression of MMP-2 in pancreatic cancer cells; and NK-1R antagonists inhibit these effects. Furthermore, SP promotes neurite outgrowth and the migration of pancreatic cancer cell cluster to the DRGs, which is blocked by NK-1R antagonists in the co-culture model. Our results suggest that SP plays an important role in the development of pancreatic cancer metastasis and PNI; and blocking the SP/NK-1R signaling system is a novel strategy for the treatment of pancreatic cancer.Molecular Cancer Research 01/2013; · 4.29 Impact Factor -
Article: Hyperglycemia as a mechanism of pancreatic cancer metastasis.
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ABSTRACT: As a vital step in the progression of cancer, metastasis poses the largest problem in cancer treatment and is the main cause of death of cancer patients. In pancreatic cancer, almost 80% of patients have locally deteriorated or metastatic disease and thus are not appropriate for resection at the time of diagnosis. Due to the high rate of incidence and mortality, it is crucial to study the molecular mechanisms of metastasis to clarify therapeutic targets to hinder the spread of cancer. Diabetes mellitus has long been considered a potential risk factor for pancreatic cancer. In this review, we comprehensively describe the role of hyperglycemia in governing critical steps of the metastatic process. In particular, we focus on the hyperglycemia-dependent aspects of the Epithelial-Mesenchymal Transition (EMT) and vascular dysfunction. Furthermore, we discuss how hyperglycemia-related production of reactive oxygen species (ROS) may play an important role in these two processes. A deep understanding of metastasis mechanisms will identify novel targets for therapeutic intervention.Frontiers in Bioscience 01/2012; 17:1761-74. · 3.52 Impact Factor -
Article: Primitive chest wall neuroectodermal tumor in a pediatric patient.
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ABSTRACT: A 13-year-old boy with a primitive neuroectodermal tumor of the chest wall is presented. After four cycles of chemotherapy, a computed tomography scan of his chest showed a larger mass invading the left upper lobe of the lung. He underwent resection of the left chest wall from the left fourth to sixth ribs, including the tumor, combined with left upper lobectomy and lymph node dissection. A diagnosis of primitive neuroectodermal tumor was confirmed histopathologically and immunohistochemically. After surgery, four cycles of chemotherapy with ifosfamide and etoposide were given. One year after treatment, the patient is currently doing well without evidence of recurrence.Interactive cardiovascular and thoracic surgery 07/2011; 13(4):440-1. -
Article: Stem cell factor/c-kit signaling enhances invasion of pancreatic cancer cells via HIF-1α under normoxic condition.
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ABSTRACT: The SCF/c-kit signaling plays an important role in invasion of c-kit-expressing tumor cells, however, the molecular mechanisms have not been studied yet. Using a pancreatic cancer model, we demonstrate that SCF/c-kit binding up-regulates the expression of invasion-related genes through the accumulation of HIF-1α. Furthermore, the expression of HIF-1α induced by SCF is not dependent on the oxygen level, but rather on both the PI3K/Akt and Ras/MEK/ERK signaling pathways. In conclusion, under normoxic conditions, SCF/c-kit binding increases expression of HIF-1α through the PI3K/Akt and Ras/MEK/ERK pathways, and the accumulation of HIF-1α up-regulates expression of invasion-related genes that augment the invasiveness of pancreatic cancer, a fatal cancer. Therefore, our results suggest that the inhibition of both c-kit and HIF-1α may be an effective strategy for pancreatic cancer therapy.Cancer letters 02/2011; 303(2):108-17. · 4.86 Impact Factor -
Article: Hyperglycemia enhances the invasive and migratory activity of pancreatic cancer cells via hydrogen peroxide.
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ABSTRACT: Diabetes mellitus and pancreatic cancer are intimately related. Hyperglycemia, a chronic abnormality in diabetes, has been proved to be an independent predictor of mortality from cancer of the pancreas. However, little is known regarding the effect of hyperglycemia on pancreatic cancer cells. The aim of the present study was to evaluate whether increases in glucose concentration modulate the invasive and migratory potential of cancer cells, contributing to their enhanced metastatic behavior. Human pancreatic cancer cells BxPC-3 and Panc-1 were cultured in 5.5, 25 or 55 mM glucose for 12, 24 or 48 h in the absence or presence of superoxide dismutase and catalase. The intracellular reactive oxygen species were determined using 2,7-dichlorodihydrofluorecein diacetate. Wound healing assay and transwell invasion assay were used to detect the migratory and invasive potential of cancer cells. The invasion-related factor, urokinase plasminogen activator, was measured by RT-PCR and Western blot analysis. The production of reactive oxygen species was increased by glucose in a concentration-dependent manner. High glucose significantly enhanced the cell migration and invasion potential. Meanwhile, the expression of urokinase plasminogen activator was also increased. Superoxide dismutase-dependent production of hydrogen peroxide led to increased cell invasive and migratory ability and the expression of urokinase plasminogen activator. These increases were reversed by the hydrogen peroxide-detoxifying enzyme catalase. These results suggest that the association between hyperglycemia and poor prognosis in pancreatic cancer can be attributed to the alterations of the migratory and invasive ability of the cells through the production of hydrogen peroxide.Oncology Reports 01/2011; 25(5):1279-87. · 1.84 Impact Factor -
Article: High glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR.
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ABSTRACT: Multiple lines of evidence suggest that a large portion of pancreatic cancer patients suffer from either hyperglycemia or diabetes, both of which are characterized by high blood glucose level. However, the underlying biological mechanism of this phenomenon is largely unknown. In the present study, we demonstrated that the proliferative ability of two human pancreatic cancer cell lines, BxPC-3 and Panc-1, was upregulated by high glucose in a concentration-dependent manner. Furthermore, the promoting effect of high glucose levels on EGF transcription and secretion but not its receptors in these PC cell lines was detected by using an EGF-neutralizing antibody and RT-PCR. In addition, the EGFR transactivation is induced by high glucose levels in concentration- and time-dependent manners in PC cells in the presence of the EGF-neutralizing antibody. These results suggest that high glucose promotes pancreatic cancer cell proliferation via the induction of EGF expression and transactivation of EGFR. Our findings may provide new insight on the links between high glucose level and PC in terms of the molecular mechanism and reveal a novel therapeutic strategy for PC patients who simultaneously suffer from either diabetes or hyperglycemia.PLoS ONE 01/2011; 6(11):e27074. · 4.09 Impact Factor -
Article: [Bronchial sleeve lobectomy and carinal resection in the treatment of central lung cancer: a report of 92 cases].
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ABSTRACT: Surgery is the best treatment for early and middle stage non-small cell lung cancer. The aim of this study is to summarize the experience of bronchial sleeve mortality lobectomy and carinal resection in the treatment of 92 patients with central lung cancer from January, 1996 to May, 2010. A total of 92 patients with central lung cancer underwent pulmonary resection. Carinal resection and reconstruction were performed in 14 patients, bronchial sleeve resection in 70 patients, and bronchial sleeve combined with pulmonary artery sleeve lobectomy in 8 patients. There was no operative mortality. The average operation time was 2 hours and 43 minutes. Postoperative complications such as pulmonary atelectasis occurred in 6.94% (7/92) of total group, and hoarseness in 4.35% (4/92). The 1, 3 and 5 year survival rates were 80.7%, 59.6% and 31.5%. Bronchial sleeve lobectomy and double sleeve lobectomy are capable of excising pulmonary tumor as much as possible while remaining healthy lung tissues. Carinal resection and reconstruction is helpful to extend the surgical indication, and increase the chance of successful resection.Zhongguo fei ai za zhi = Chinese journal of lung cancer 11/2010; 13(11):1056-8. -
Article: Upregulation of uncoupling protein-3 in skeletal muscle during exercise: a potential antioxidant function.
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ABSTRACT: Uncoupling protein-3 (UCP3) expression has been shown to increase dramatically in response to muscular contraction, but the physiological significance of UCP3 upregulation is still elusive. In this study, UCP3 mRNA and protein expression were investigated along with mitochondrial respiratory function, reactive oxygen species (ROS) generation, and antioxidant defense in rat skeletal muscle during and after an acute bout of prolonged exercise. UCP3 mRNA expression was elevated sharply at 45 min of exercise, reaching 7- to 8-fold above resting level at 150 min. The increase in UCP3 protein content showed a latent response but was elevated approximately 1.9-fold at 120 min of exercise. Both UCP3 mRNA and UCP3 protein gradually returned to resting levels 24 h postexercise. Mitochondrial ROS production was progressively increased during exercise. However, ROS showed a dramatic drop at 150 min although their levels remained severalfold higher during the recovery. Mitochondrial State 4 respiration rate was increased by 46 and 58% (p < 0.05) at 90 and 120 min, respectively, but returned to resting rate at 150 min, when State 3 respiration and respiratory control index (RCI) were suppressed. ADP-to-oxygen consumption (P/O) ratio and ATP synthase activity were lowered at 3 h postexercise, whereas proton motive force and mitochondrial malondialdehyde content were unchanged. Manganese superoxide dismutase gene expression was not affected by exercise except for an increase in mRNA abundance at 3 h postexercise. These data demonstrate that UCP3 expression in rat skeletal muscle can be rapidly upregulated during prolonged exercise, possibly owing to increased ROS generation. Increased UCP3 may partially alleviate the proton gradient across the inner membrane, thereby reducing further ROS production by the electron transport chain. However, prolonged exercise caused a decrease in energy coupling efficiency in muscle mitochondria revealed by an increased respiration rate due to proton leak (State 4/State 3 ratio) and decreased RCI. We thus propose that the compromise of the oxidative phosphorylation efficiency due to UCP3 upregulation may serve an antioxidant function to protect the muscle mitochondria from exercise-induced oxidative stressFree radical biology & medicine 11/2008; 46(2):138-45. · 5.42 Impact Factor -
Article: [Clinical analysis of surgical treatment results in 13 patients with primary trachea tumor.].
Zhongguo fei ai za zhi = Chinese journal of lung cancer 06/2008; 11(3):447-8. -
Article: Regulation of mitochondrial uncoupling respiration during exercise in rat heart: role of reactive oxygen species (ROS) and uncoupling protein 2.
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ABSTRACT: The physiological significance of cardiac mitochondrial uncoupling protein 2 (UCP2)-mediated uncoupling respiration in exercise is unknown. In the current study, mitochondrial respiratory function, UCP2 mRNA level, UCP2-mediated respiration (UCR), and reactive oxygen species (ROS) generation, as well as manganese superoxide dismutase (MnSOD) activity were determined in rat heart with or without endurance training after an acute bout of exercise of different duration. In the untrained rats, state 4 respiration and UCR-independent respiration rates were progressively increased with exercise time and were 64 and 70% higher, respectively, than resting rate at 150 min, whereas UCR was elevated by 86% with no significant change in state 3 respiration. UCP2 mRNA level showed a 5- and 4-fold increase, respectively, after 45 and 90 min of exercise, but returned to resting level at 120 and 150 min. Mitochondrial ROS production and membrane potential (Deltapsi) increased progressively until 120 min, followed by a decrease to the resting level at 150 min. MnSOD mRNA abundance showed a 2-fold increase at 120 min but MnSOD activity did not change with exercise. Training significantly increased mitochondrial ATP synthetase activity, ADP to oxygen consumption (P/O) ratio, respiratory control ratio, and MnSOD activity, whereas exercise-induced state 4 respiration, UCR, ROS production, and Deltapsi were attenuated in the trained rats. We conclude that (1) UCP2 mRNA expression and activity in rat heart can be upregulated during prolonged exercise, which may reduce cross-membrane Deltapsi and thus ROS production; and (2) endurance training can blunt exercise-induced UCP2 and UCR, and improve mitochondrial efficiency of oxidative phosphorylation due to increased removal of ROS.Free Radical Biology and Medicine 05/2008; 44(7):1373-81. · 5.42 Impact Factor -
Article: Effects of soybean isoflavone dosage and exercise on the serum markers of bone metabolism in ovariectomized rats.
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ABSTRACT: This study was designed to determine whether combined treatments with soybean isoflavone dosage and moderate exercise would exhibit synergistically effects on bone metabolism following the onset of menopause. Fifty 12 wk-old female Wistar rats were assigned to five groups: 1) Sham operated (Sham), 2) ovariectomized (OVX), 3) OVX received soybean isoflavone (OVX-IF), 4) OVX exercised (OVX-EXE) and 5) OVX treated with both soybean isoflavone and exercise (OVX-IF-EXE). All rats were fed a normal diet ad libitum. Daily soybean isoflavone dosage was 50 mg/kg body weight. The vehicle was given in Sham, OVX and OVX-EXE groups. The drugs were all oral administered using a stomach tube. Exercising rats were trained on an uphill treadmill at 20 m/min for 1h/day, 5 days/week. The experimental duration consisted of the adaptation periods of 2 weeks and treatment periods of 8 weeks. The results showed that the uterus relative weights in OVX-EXE, OVX-IF and OVX-IF-EXE groups were all lower than those in Sham, they were higher than those in the OVX group. Serum alkaline phosphates (AKP) activities of OVX was significantly increased as compared to that of Sham (p<0.01). OVX-IF and OVX-IF-EXE respectively decreased the Serum alkaline phosphates activities, as compared to that of OVX (p<0.01). The tartrate-resistant acid phosphatase (TRAP) value of OVX was significantly increased as compared to that of Sham (p<0.05). OVX-IF decreased the TRAP as compared to that of OVX (p<0.05). These results suggest soybean isoflavone and resistance exercise both can restrain ovx-induced bone loss. But their mechanisms may be different.Asia Pacific Journal of Clinical Nutrition 01/2007; 16 Suppl 1:193-5. · 1.13 Impact Factor -
Article: Radionuclide Colloid 32P Used for the Treatment of Stage II Lung Cancer by Video Enhanced Minimal Access Muscle Sparing Thoracotomy
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ABSTRACT: Objective: To study the feasibility of radionuclide colloid 32p used for the treatment of stage II lung cancer by video enhanced minimal access muscle sparing thoracotomy (VEMAST). Methods: Video assisted thoracoscopic surgery (VATS) was carried out under general anesthesia. A double lumen endobronchial tube was intubated into trachea. One lung ventilation of the healthy side was done during operation. An incision of 8-10 cm long was made along the 4th or 5th intercostals. The lobectomy could be performed under VATS. Radionuclide colloid 32p was injected locally into the area where surgical cleaning of lymph node around was considered to be unsatisfactory or desection of the tumor was not completed. Results: The operation with VEMAST was successful in 29 patients. A conventional lobectomy by thoracotomy had to be done due to unusual bleeding from the pulmonary artery involved during VEMAST in one case and the procedure was interrupted because the pulmonary artery cloud not be separated from the tumor in another patient. There was no dead case or the patient who had any severe complication or adverse response to the radiant. Conclusion: Radionuclide therapy was performed to the treatment of stage II lung cancer with VEMAST in case that surgical resection was considered not to be satisfactory. Minithoractomy assisted with VATS lobectomy and radionuclide colloid 32p therapy is a safe and effective technique for some selected stage II lung cancer.The Chinese-German Journal of Clinical Oncology 05/2004; 3(2):122-123.
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Institutions
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2011–2013
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Xi'an Jiaotong University
- Department of Hepatobiliary Surgery
Xi’an, Shaanxi Sheng, China
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