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Objective To investigate the expressions of LYVE-1 and PROX-1 in human breast carcinoma and the clinical significance of lymphatic vessel density.Methods Immunohistochemistry (SP method)was used to detect the expressions of LYVE-1 and PROX-1 in 80 specimens of breast invasive ductal carcinoma and 35 specimens of breast hyperplasia.Results The density of lymphatic vessels positive for LYVE-1 or PROX-1 was significantly higher in breast carcinoma than in breast hyper-plasia (P<0.01).There was a significant correlation between lymphatic vessel density and lymph node metastasis (P<0.01). A negative correlation was noted between the PROX-1 expression in carcinoma cells and tumor grade (P<0.01)or TNM stage (P < 0.01 ).Conclusion Lymphangiogenesis is increased in breast carcinoma,which is associated with lymph node metastasis.PROX-1 may be involved in tumorigenesis,progression and lymphatic metastasis in breast cancer.
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The aim of the present study was to examine the effects of suppression of EphB4 and/or mTOR on the biological behaviors of ovarian cancer cells, and the potential regulatory pathways. Antisense EphB4 vectors and shRNA vectors targeting mammalian target of rapamycin (mTOR) were constructed and transfected into A2780 and SKOV3 cells (two ovarian cancer cell lines). The effects of the antisense EphB4 vectors and the shRNA vectors on the proliferation, apoptosis and invasion of ovarian cancer cells were measured, and the expression of EphB4, mTOR and Akt detected. The results showed that transfection with mTOR shRNA could inhibit growth, induce apoptosis, and reduce invasive ability of ovarian cancer cells, which was accompanied by downregulation of EphB4, mTOR and Akt. The inhibitory effects on cell growth caused by mTOR shRNA alone were weaker than those by antisense pEGFP-C1-EphB4. In the antisense pEGFP-C1-EphB4-transfected cells, it was found that EphB4 knockdown could decrease the mTOR expression and slightly reduce the Akt phosphorylation. Significant suppressive effects on cell growth were observed in cells co-transfected with antisense pEGFP-C1-EphB4 and mTOR shRNA. In co-transfection group, the expression levels of EphB4, mTOR and Akt were distinctly lower than those in other groups. It was concluded that suppression of EphB4 may inhibit the growth of ovarian cancer cells by downregulation of the PI3K/Akt/mTOR pathway, and reverse Akt phosphorylation induced by mTOR shRNA. Inhibition of EphB4 and mTOR combined may cooperatively suppress the biological behaviors of ovarian cancer cells.
Assuntos
Feminino , Humanos , Apoptose , Genética , Linhagem Celular Tumoral , Proliferação de Células , Regulação para Baixo , Genética , Neoplasias Ovarianas , Patologia , Proteínas Proto-Oncogênicas c-akt , Genética , Metabolismo , RNA Interferente Pequeno , Genética , Receptor EphB4 , Genética , Metabolismo , Supressão Genética , GenéticaRESUMO
The aim of the present study was to examine the effects of suppression of EphB4 and/or mTOR on the biological behaviors of ovarian cancer cells, and the potential regulatory pathways. Antisense EphB4 vectors and shRNA vectors targeting mammalian target of rapamycin (mTOR) were constructed and transfected into A2780 and SKOV3 cells (two ovarian cancer cell lines). The effects of the antisense EphB4 vectors and the shRNA vectors on the proliferation, apoptosis and invasion of ovarian cancer cells were measured, and the expression of EphB4, mTOR and Akt detected. The results showed that transfection with mTOR shRNA could inhibit growth, induce apoptosis, and reduce invasive ability of ovarian cancer cells, which was accompanied by downregulation of EphB4, mTOR and Akt. The inhibitory effects on cell growth caused by mTOR shRNA alone were weaker than those by antisense pEGFP-C1-EphB4. In the antisense pEGFP-C1-EphB4-transfected cells, it was found that EphB4 knockdown could decrease the mTOR expression and slightly reduce the Akt phosphorylation. Significant suppressive effects on cell growth were observed in cells co-transfected with antisense pEGFP-C1-EphB4 and mTOR shRNA. In co-transfection group, the expression levels of EphB4, mTOR and Akt were distinctly lower than those in other groups. It was concluded that suppression of EphB4 may inhibit the growth of ovarian cancer cells by downregulation of the PI3K/Akt/mTOR pathway, and reverse Akt phosphorylation induced by mTOR shRNA. Inhibition of EphB4 and mTOR combined may cooperatively suppress the biological behaviors of ovarian cancer cells.
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TMTP1, a 5-amino acid peptide NVVRQ, obtained by using the flagella peptide library screening in our previous studies, can be used for the labeling of malignant in situ and metastatic lesions, and even micro-metastases. In this study, TMTP1 was assessed for its ability to specifically target the malignant hematopoietic cells and metastatic lesions of hematological malignancies. FITC-TMTP1 was chemically synthesized. Immunofluorescence assay and competitive test were carried out to determine the specific binding capacity of TMTPl to hematological malignant cell lines, including HL60, k562, SHI-1, Jurkat, Raji, El-4 and umbilical cord blood mononuclear cells. Mononuclear cells were isolated from the bone marrow of healthy subjects and patients with chronic myeloid leukemia. Then the cells were co-clutured with TMTP1 or scrambled peptides and the binding and affinity of TMTP1 peptide to the primary cells of hematological malignancies were flow cytometrically analyzed. The binding specificity of TMTP1 to target hematological malignancies was measured in vivo by intravenous injection of FITC-conjugated TMTP1 into El-4 lymphoma-bearing mice. The results showed that TMTP1 specifically bound to the cells of a series of hematological malignancies, including HL60, k562, Jurkat, Raji, El-4 and chronic myeloid leukemia primary cells but not to bone marrow mononuclear cells from healthy subjects. By contrast, TMTP1 could bind to the metastatic foci of lymphoma originating from the EL-4 cell line while the scrambled peptide failed to do so. Moreover, the occult metastases could be identified, with high specificity, by detecting FITC-TMTP1. We are led to conclude that TMTP1, as a novel tumor-homing peptide, can serve as a marker for primary malignant and metastatic lesions for the early diagnosis of hematological malignances and a carrier of anticancer drugs for cancer treatment.
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Objective To investigate the therapeutic effect of Chinese herbal medicine for seminal delayed liquefaction(SDL).Methods Two hundred and ninety SDL patients were randomized into two groups.Group A(N=230)received oral use of yin-nourishing and blood-activating herbal medicine(mainly composed of Radix Ophiopogonis,Radix Scrophulariae,Fructus Ligustri Lucidi,Herba Ecliptae,Radix Salviae Miltiorrhizae,Flos Carthami,Rhizoma Sparganii,Eupolyphaga seu Steleophaga),and group B(N=60)received intramuscular injection of chymotrypsin and oral use of vitamin C and zinc gluconate.The therapeutic effect in the two groups were evaluated after treatment,and the changes of main parameters of seminal liquid as well as the seminal plasma contents of prostate specific antigen(PSA),acid phosphatase(AP),citric acid(CA)and zinc were observed before and after treatment.Results In group A,156 patients were cured,57 effective,17 ineffective and the total effective rate was 92.6%;in group B,21 patients were cured,17 effective,22 ineffective and the total effective rate was 63.3%.The Therapeutic effect was better in group A than that in group B(P