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Objective: To study the expression and significance of VEGF-C, D2-40, and E-Cad in Human breast carcinoma. Methods: S-P immunohistochemical method was used to assess the expression of VEGF-C in 88 cases of infiltrating ductal carcinoma of the breast (with intact clinicopathologic and follow-up in-formation) and 54 cases of different intraductal hyperplastic lesions. The relationship of VEGF-C expression with D2-40 and E-Cadherin in infiltrating ductal carcinoma of the breast was analyzed. Results: VEGF-C ex-pression was higher in the invasive group than that in the dysplasia group and benign lesions. VEGF-C ex-pression in the metastatic group was significantly higher than that in the group without lymph node metasta-sis, indicating that VEGF-C plays an important role in the growth and metastasis of breast cancer. VEGF ex-pression in breast cancer group was higher than that in the dysplasia group and benign lesions. LVD count in the group with lymph node metastasis was significantly higher than that in the group without lymph node me-tastasis. The positive rate of E-Cad expression in the invasive group was significantly lower than that in the dysplasia group and benign lesions. VEGF-C expression was positively correlated with D2-40 expression. VEGF-C expression was negatively correlated with E-Cad expression. Conclusion: VEGF-C and D2-40 could be used for the detection of early lymphatic metastasis of breast cancer. VEGF-C and E-Cad can be used as important indices for the evaluation of the prognosis of breast cancer.
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Aim To observe the effects of amlodipine on cell cycle,cell cycle-related genes and cyclin expression of human breast carcinoma MCF-7 cells.And to probe effects of amlodipine on cell cycle and its mechanism of human breast carcinoma MCF-7 cells.Methods In vitro growth inhibitory effects of amlodip-ine on human breast carcinoma MCF-7 cells were determined by MTT assay,cell cycle distribution was detected by flow cytometry,the Mrna expression levels of cell cycle-related genes cyclinD1 and p21 were treated by RT-PCR,and the protein expression of cell cycle protein cyclinD1 and p21 were assessed by Western blot.Results With dose and time dependently,amlodipine could inhibit the proliferation of human breast carcinoma MCF-7 cells in vitro.The IC_(50) was 14.439 μmol·L~(-1).When breast cancer cells MCF-7 were treated with 7.22 μmol·L~(-1)(1/2 IC_(50)),14.439 μmol·L~(-1)(IC_(50))and 28.88 μmol·L~(-1)(2IC_(50))amlodipine for 48 h,the ratios in the G_0/G_1 phase were significantly increased as compared with control group(P<0.05).Amlodipine inhibited the expression of Mrna and protein of cyclinD1,while increased the expression of Mrna and protein of p21.Conclusions Amlodipine exhibits obvious anti-tumor activities on human breast carcinoma MCF-7 cells and arrest cell cycle in G_1 phase.The mechanism of G_1 phase arresting may be related to modulating the Mrna and protein expression of cell cycle-related gene cyclinD1 and p21.
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The aim of present study was to investigate the effects of kaempferol on cellular proliferation and cell cycle arrest and explore the mechanism for these effects in human breast carcinoma MDA-MB-453 cells. Cells were treated with kaempferol at various concentrations (ranging from 1 to 200 microM) for 24 and 48 hrs. Kaempferol significantly inhibited cancer cell growth in cells exposed to 50 and 10 microM of kaempferol and incubated for 24 and 48 hrs, respectively. Exposure to kaempferol resulted in cell cycle arrest at the G2/M phase. Of the G2/M-phase related proteins, kaempferol down-regulated CDK1 and cyclin A and B in cells exposed to kaempferol. In addition, small DNA fragments at the sub-G0 phase were increased by up to 23.12 and 31.90% at 10 and 50 microM incubated for 24 and 48 hrs, respectively. The kaempferol-induced apoptosis was associated with the up-regulation of p53. In addition, the phosphorylation of p53 at the Ser-15 residue was observed with kaempferol. Kaempferol inhibits cell proliferation by disrupting the cell cycle, which is strongly associated with the induction of arrest at G2/M phase and may induce apoptosis via p53 phosphorylation in human breast carcinoma MDA-MB-453 cells.
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Humans , Apoptosis , Breast , Breast Neoplasms , Cell Cycle , Cell Cycle Checkpoints , Cell Proliferation , Cyclin A , DNA , Kaempferols , Phosphorylation , Proteins , Up-RegulationABSTRACT
Objective To investigate ectopic expression of key elements of Wnt/?-catenin signaling pathway,including E-cadherin,?-catenin and Cyclin D1,as well as the relationship between ectopic expression of ?-catenin and overexpression of Her2 in human breast carcinoma tissues.Methods Immunohistochemical technique(Elivision) was used to detect the expression of Her2 and three elements of Wnt/?-catenin signaling pathway(?-catenin,E-cadherin,Cyclin D1) in 90 samples of human breast carcinoma.Results In E-cadherin normally-expressed group,the ectopic expression rate of ?-catenin(27.3%) was significantly lower than that(75.0%) in E-cadherin negative breast carcinoma;in ?-catenin ectopic expression group,overexpression rate of Cyclin D1(83.3%) was significantly higher than that(40.7%) in the other group.In Her2 overexpressed-breast carcinoma tissue,the ectopic expression rate of ?-catenin(73.5%) was significantly higher than that(19.6%) in Her2 negative breast carcinoma.Her2 overexpression could coexist with ectopic expression of Wnt/?-catenin in promoting axillary lymph node metastasis in human breast carcinoma.Conclusion Ectopic expression of Wnt/?-catenin signaling pathway does exist in some human breast carcinoma tissues,and the abnormal expression correlates with overexpression of Her2.Furthermore,the instantaneous activation of them could present synergism in promoting metastasis of axillary lymph nodes.
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Background and purpose:18?-glycyrrhetinic acid(GA) is one of the important components of glycyrrhiza.Recent years,studies showed that GA has the effect of proliferation inhibition in human acute lymphoblastic leukemia cells,human liver carcinoma and lung cancer cells.We investigated the effects of GA on induction of apoptosis in human breast carcinoma(MCF7) cells.The previous studies have demonstrated that the dynamic change of intracellular free Ca~(2+) concentration([Ca~(2+)]i)plays important roles in many links of apoptosis-induced process.Therefore we also researched the relationship between GA-induced apoptosis and [Ca~(2+)]i in MCF-7 cells.Methods:After MCF-7 cells were treated with 50-250 ?mol/L GA for 24 h,cell viability for proliferation was assessed by MTT assay.MCF-7 cells treated with 100 ?mol/L and 150 ?mol/L GA for 24 h,the apoptotic rates in MCF7 cells were examined by terminal deoxynucleotide transferase mediated dUTP nick-end-labeling method,flow cytometry with Annexin V/ propidium iodide fluorescent stain and single cell gel electrophoresis assay(SCGE).For cells treated with 150 ?mol/L GA for 24 h,i was measured by Fure-2 fluorescein load method.For cells treated with 150 ?mol/L GA combined with 100 ?mol/L BAPTA-AM or 0.5 mmol/L EGTA for 24 h,cell apoptosis were examined by SCGE.Results:For cells treated with GA from 100 ?mol/L to 250 ?mol/L,the rate of proliferative inhibition was increased significantly(P
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By electron microscopic observation,we found few pit cells in liver,spleen.lungs,and small intestine in Wistar rat.The pit cells show several morphologicalcharacteristics as follows:1.electron dense granules in cytoplasm,which aresurrounded by a limiting membrane;2.vesicles with rod shaped bodies incytoplasm;3.eccentric nucleus with marginal heterochromatin;4.well developedpseudopodia.In addition,the pit cells have also been found in breast carcinoma in3 patients.According to their distribution and morphology,we preliminarilydeduced they probably belong to natural killer cells and may act as a cytotoxicagent and an immunological defender against carcinoma.