Basic Medical Institute
Basic Medical Institute
Liu L.,Basic Medical Institute |
Zhao E.,Affiliated Hospital of Chengde Medical College |
Li C.,Affiliated Hospital of Chengde Medical College |
Huang L.,Affiliated Hospital of Chengde Medical College |
And 5 more authors.
Cancer Epidemiology | Year: 2013
TRIM28 is a universal corepressor for Kruppel-associated box zinc finger proteins. In this study, we demonstrated the expression of TRIM28 gene was significantly higher in cancerous tissues than in noncancerous tissues (P<. 0.001). TRIM28 knockdown resulted in a decrease in cell proliferation in liquid media as well as in soft agar. The proliferation rate was impaired and the cell cycle progression was inhibited after knockdown of TRIM28 in non-small cell lung cancer cell lines PAa and SK-MES-1. We used real-time polymerase chain reaction to detect circulating cancer cells in 138 non-small cell lung cancer patients. The overall positive detection rate was 30.4% (42 of 138) in peripheral blood of NSCLC patients and was 29.9% (29 of 97) in early-stage patients. In a 70-month follow-up study, 20 of 29 patients (69.0%) in TRIM28 positive group had recurrence and/or metastasis, significantly higher (P= 0.004) than in the TRIM28 negative group (25 of 68, 36.8%). In addition, non-small cell lung cancer patients whose circulating cancer cells expressed TRIM28 suffered shorter tumor-specific survival compared with those with absent TRIM28 expression (P<. 0.001). Results of our study showed that TRIM28 provides a survival advantage to lung cancer cells and may be a new marker to predict metastasis and prognosis in early-stage non-small cell lung cancer patients. © 2012 Elsevier Ltd.
Ma Y.-C.,Basic Medical Institute |
Fan W.-J.,Basic Medical Institute |
Wu H.,Basic Medical Institute |
Wang F.-Q.,Basic Medical Institute
Acta Anatomica Sinica | Year: 2014
Objective: To clarify Notch signaling in platelet derived growth factor-BB (PDGF-BB) induced proliferation of human pancreatic adenocarcinoma (HPAC). Methods: After being treated by PDGF-BB and (or) 7-secretase inhibitor DAPT, changes of HPAC cell proliferation were detected by MTT assay; Alterations of Notch level in HPAC cells were measured by Western blotting assay; Variations of capability in cardiolipin synthetic lecithin (CSL) binding to the promoter of target gene hes-1 were identified by chromatin immunoprecipitation (CHIP) assay. Results: PDGF-BB facilitates the proliferation of HPAC cells, upregulates Notch level and enhances the capability in CSL binding to the promoter of hes-1. DAPT and PDGFR inhibitor treatment suppresses and invalidates PDGF-BB effection. Conclusion: Notch-1 signaling plays an essential role in the modulation of PDGF-BB-induced proliferation of HPAC cells.
Li X.,Basic Medical Institute |
Chen X.,Hebei Normal University |
Wang X.-J.,Basic Medical Institute |
Lu G.-B.,Basic Medical Institute |
Gao F.-L.,Hebei Normal University
Acta Anatomica Sinica | Year: 2010
Objective: To study whether annexin A7 (ANXA7) low expression can affect apoptosis and proliferation of HeLa cells. Methods: Western blotting was used to identify whether siRNA can highly surpress annexin A7 expressin. When the effect of the siRNA was assured, the siRNA was transfected into HeLa cells by lipofectamine 2000. At the same time, cells in negative control group were transfected negative siRNA while cells as blank control group did not receive any treatment. After transfection for 48 hours, resazurin assay was conducted and DNA content was analyzed by cytometry. Results: Resazurin assay showed that proliferation of the siRNA interference cell group decreased significantly (P < 0.05). Cytometry test showed that apoptosis of the siRNA interference group increased obviously (P < 0.05). Conclusion: ANXA7 low expression may affect proliferation and apoptosis of HeLa cells.
Zhang J.,Basic Medical Institute |
Deng Z.,Basic Medical Institute |
Liao J.,Basic Medical Institute |
Song C.,Basic Medical Institute |
And 5 more authors.
Journal of Cerebral Blood Flow and Metabolism | Year: 2013
The purpose of this study was to investigate the protective mechanism of leptin-mediated metabolic recovery against cerebral injury after ischemia and reperfusion. We determined the neurologic deficit score, extent of brain edema, and infarct volume after reperfusion. The histopathologic alterations and changes in glucose uptake in the brain were also observed. Moreover, the levels of lactate dehydrogenase (LDH), lactic acid, pyruvate, and ATP in brain tissue were detected. Leptin levels in serum were also detected. To further define leptin-induced neuroprotective signaling pathways, we examined the levels of phosphorylated Akt (p-Akt) in the brain and in cultured cells. After transient ischemia, leptin treatment markedly reduced the neurologic deficits, cerebral infarct volume, and brain edema. After leptin injection, ATP, leptin, and p-Akt levels were significantly increased, LDH levels and lactic acid/pyruvate ratio were noticeably reduced, and histopathologic injuries were alleviated, which were all reversed by the PI3 K inhibitor LY294002. These data show that leptin ameliorates cerebral ischemia/reperfusion injury by enhancing p-Akt, which in turn improves the supply of energy. The PI3 K/Akt pathway was found to be the critical pathway for the mediation of leptin-induced neuroprotection, a finding that may prove to be useful in the treatment of ischemic stroke. © 2013 ISCBFM All rights reserved.
Liu L.,Basic Medical Institute |
Ma C.,Basic Medical Institute |
Xu Q.,Basic Medical Institute |
Cheng L.,Basic Medical Institute |
And 5 more authors.
Oncology Letters | Year: 2014
The aim of the present study was to develop a simple and rapid method for the detection of circulating cancer cells using multiple tumor markers and to investigate the clinical significance of circulating cancer cells in breast cancer patients. A novel rapid nested polymerase chain reaction (PCR) assay, with high sensitivity and specificity, was evaluated, which was considered to be suitable for clinical application. The rapid nested PCR method was used to detect the circulating cancer cells of 142 breast cancer patients, using a panel of marker genes (FAM83A, NPY1R and KRT19), which were identified by the Digital Gene Expression Displayer Tool of the National Cancer Institute-Cancer Genome Anatomy Project. In total, 79.6% of the 142 breast cancer patient blood samples were found to express at least one tumor marker. In addition, the number of positive markers was found to significantly correlate with the disease stage and presence of distant metastasis. Furthermore, positivity for more than one tumor marker appeared to predict a reduced survival time in breast cancer patients.
Tian H.,Basic Medical Institute |
Liang X.,Basic Medical Institute |
Wang X.,Basic Medical Institute |
Chen L.,Basic Medical Institute |
Li X.,Basic Medical Institute
Chinese Journal of Cancer Biotherapy | Year: 2015
Objective: To investigate the effect of ANXA7 on the proliferation and apoptosis of human stomach carcinoma MGC-803 cells by downregulating ANXA7 expression using RNA interference technique. Methods: The MGC-803 cells were transfected with lipofectineTM2000 alone (blank control), scrambled siRNA (negative control), and siRNA targeted ANXA7 (experiment group). After 48 hours, ANXA7 expression was examined by immunoblotting. The proliferation and growth of transected cells were assessed by MTT and colony formation assays. Apoptosis of the cells was analyzed by flow cytometry. Results: The expression of ANXA7 was significantly decreased in cells transfected with ANXA7 siRNA compared with these in the two controls [(21.79±1.72)% vs (99.87±5.13)% and (93.45±4.89)%, P <0.05]. When ANXA7 expression was decreased, the proliferation and colony formation abilities of MGC-803 cells were markedly inhibited [(0.97±0.06) vs (1.21±0.07) and (1.25±0.08), P <0.05; and (183±21) vs (363±35) and (348±27), P <0.05], whereas the apoptosis of the cells was not affected statistically [P >0.05]. Conclusion: ANXA7 regulates the proliferation and colony formation of MGC-803 cells, and appears not involved in their apoptosis. © 2015, Editorial office of Chinese Journal of Cancer Biotherapy. All rights reserved.
Liu L.,Chengde Medical College |
Xu Q.,Basic Medical Institute |
Cheng L.,Chengde Medical College |
Ma C.,Chengde Medical College |
And 5 more authors.
Oncology Letters | Year: 2015
The aim of the current study was to evaluate a novel tumor marker, neuropeptide Y receptor Y1 (NPY1R), for the detection of circulating cancer cells and to investigate its clinical significance in breast cancer patients. The Digital Gene Expression Displayer tool of the Cancer Genome Anatomy Project was used to identify the marker gene NPY1R, which is able to detect circulating cancer cells. Nested quantitative polymerase chain reaction was performed to correlate the NPY1R expression levels with the clinicopathological features of 142 breast cancer patients. A follow-up study of 131 of the breast cancer patients was conducted for 38 months. Compared with the 60 normal control individuals, NPY1R was highly expressed in the cancer patients (P<0.01). These high levels of NPY1R expression were positively correlated with the clinical stage and lymph node metastasis status of the disease, as well as with the status of the estrogen and progesterone receptors (P<0.05). Breast cancer patients with circulating cancer cells that expressed NPY1R exhibited shorter tumor-specific survival when compared with those with no NPY1R expression (P<0.01). Additionally, the mortality rate was associated with HER2 expression in the NPY1R positive and negative groups. These results indicate that NPY1R may serve as a useful marker to predict breast cancer metastasis and to evaluate the prognosis of breast cancer patients. © 2015, ONCOLOGY LETTERS. All rights reserved.
Huanna T.,Hebei University |
Huanna T.,Basic Medical Institute |
Tao Z.,Hebei University |
Xiangfei W.,Hebei University |
And 11 more authors.
Molecular Carcinogenesis | Year: 2015
Aberrant glycosylation is a hallmark of most human cancers and affects many cellular properties, including cell proliferation, apoptosis, differentiation, transformation, migration, invasion, and immune responses. Here, we report that N-acetylgalactosaminyltransferase14 (GALNT14), which mediates the initial step of mucin-type O-glycosylation and is heterogeneously expressed in most breast cancers, plays a critical role in the invasion and migration of breast cancers by regulating the activity of MMP-2 and expression of some EMT genes. We have modulated the expression of GALNT14 by RNAi and overexpression in MCF-7 cells. Overexpression of GALNT14 significantly enhanced cell migration and invasion and promoted the proliferation of breast cancer cells. Knockdown of GALNT14 reduced clonogenicity and attenuates cell migration and cell invasion. The mRNAs for N-cadherin, vimentin, E-cadherin, MMP-2, VEGF, and TGF-β were determined by RT-qPCR involving GALNT14-overexpressing or knockdown MCF-7 cells. Expression profiling revealed the upregulation of N-cadherin, vimentin, MMP-2, VEGF, TGF-β and the downregulation of E-cadherin in GALNT14 overexpressing cells, with the opposite seen in GALNT14 knockdowns. Gelatin zymography analysis further indicated that overexpression of GALNT14 increased MMP-2 activity in MCF-7 cells. Conversely, downregulation of GALNT14 reduced MMP-2 activity. Promoter analysis revealed that GALNT14 stimulates MMP-2 expression through the AP-1-binding site. Western blot analyses showed that knockdown of GALNT14 significantly reduced the expression of an oncoprotein mucin 1 (MUC1). These findings indicate that GALNT14 contributes to breast cancer invasion by altering the cell proliferation, motility, expression levels of EMT genes, and by stimulating MMP-2 activity, suggesting GALNT14 may be a potential target for breast cancer treatment. © 2015 Wiley Periodicals, Inc.
PubMed | Basic Medical Institute and Chinese PLA General Hospital
Type: Journal Article | Journal: Oncology letters | Year: 2014
Cisplatin/pemetrexed chemotherapy has been established as a standard treatment in lung adenocarcinoma. However, the response to the cisplatin/pemetrexed combination varies considerably among patients due to individual variations. Thus, novel biomarkers are required to aid the prediction of the response to the cisplatin/pemetrexed combination. We hypothesized that leptin expression may be a determinant for prognosis in lung adenocarcinoma patients with cisplatin/pemetrexed chemotherapy. Serum from consenting patients with lung adenocarcinoma were obtained for the measurement of leptin and associated tumor biomarkers. Leptin expression was measured by radioimmunoassay. Carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), CA15-3, CA125, CA72-4, cytokeratin 19 fragment (CYFRA21-1) and neuron-specific enolase (NSE) expression were determined by electrochemiluminescence immunoassays. Serum squamous cell carcinoma antigen levels were measured using a microparticle enzyme immunoassay. The associations between serum leptin and tumor biomarker expression were evaluated by Spearmans correlation analysis. Serum CEA, CA19-9, CA15-3, CA125, CA72-4, CYFRA21-1 and NSE levels showed no obvious difference among patients. However, a trend towards an improved prognosis was observed in patients with lower serum leptin at diagnosis and an increase during cisplatin/pemetrexed chemotherapy. The results indicated that the serum leptin level has prognostic indications in patients with advanced lung adenocarcinoma during cisplatin/pemetrexed chemotherapy, which indicates that it may be a useful marker for the prognosis of cancer patients undergoing chemotherapy treatment.
PubMed | Basic Medical Institute
Type: Journal Article | Journal: Cancer epidemiology | Year: 2013
TRIM28 is a universal corepressor for Kruppel-associated box zinc finger proteins. In this study, we demonstrated the expression of TRIM28 gene was significantly higher in cancerous tissues than in noncancerous tissues (P < 0.001). TRIM28 knockdown resulted in a decrease in cell proliferation in liquid media as well as in soft agar. The proliferation rate was impaired and the cell cycle progression was inhibited after knockdown of TRIM28 in non-small cell lung cancer cell lines PAa and SK-MES-1. We used real-time polymerase chain reaction to detect circulating cancer cells in 138 non-small cell lung cancer patients. The overall positive detection rate was 30.4% (42 of 138) in peripheral blood of NSCLC patients and was 29.9% (29 of 97) in early-stage patients. In a 70-month follow-up study, 20 of 29 patients (69.0%) in TRIM28 positive group had recurrence and/or metastasis, significantly higher (P = 0.004) than in the TRIM28 negative group (25 of 68, 36.8%). In addition, non-small cell lung cancer patients whose circulating cancer cells expressed TRIM28 suffered shorter tumor-specific survival compared with those with absent TRIM28 expression (P < 0.001). Results of our study showed that TRIM28 provides a survival advantage to lung cancer cells and may be a new marker to predict metastasis and prognosis in early-stage non-small cell lung cancer patients.