AIM To investigate the expression of annexin A5 in serum and tumor tissue of patients with colon cancer and to analyze its clinical significance.METHODS Ninety-three patients with colon cancer treated at our hospital ...AIM To investigate the expression of annexin A5 in serum and tumor tissue of patients with colon cancer and to analyze its clinical significance.METHODS Ninety-three patients with colon cancer treated at our hospital between February 2013 and March 2016 were included in an observation group, and 40 healthy individuals were included in a control group. Enzyme-linked immunosorbent assay was performed to determine the serum level of annexin A5, while immunohistochemistry was performed to determine the expression of annexin A5 in cancer tissues.RESULTS The serum level of annexin A5 was 0.184 ± 0.043 ng/m L in the observation group, which was significantly higher than that in the control group(P < 0.05). Annexin A5 expression was detected in 79.31% of the patients with lymph node metastasis, which was significantly higher than that in patients without lymph node metastasis(P < 0.05). Moreover, annexin A5 expression was detected in 86.96% of the patients with stage Ⅲ to Ⅳ disease, which was significantly higher than that in patients with stage Ⅰ to Ⅱ disease(P < 0.05). The serum level of annexin A5 was 0.215 ± 0.044 ng/m L in patients whose tumors were positive for annexin A5 expression, which was significantly higher than that in patients whose tumors were negative for annexin A5 expression(P < 0.05). The serum level of annexin A5 was correlated with annexin A5 expression in colon cancer tissues(r= 0.312, P < 0.05). When a cutoff value of > 0.148 ng/m L for serum level of annexin A5 was used in the diagnosis of colon cancer, the sensitivity was 83.90%, and the specificity was 57.50%.CONCLUSION For patients with colon cancer, annexin A5 expression in cancer tissues is related to lymph node metastasis and tumor grade. Serum level of annexin A5 is related to annexin A5 expression in cancer tissues and is of diagnostic relevance.展开更多
This study was to investigate the effect of annexin A5 on testosterone secretion from primary rat Leydig cells and the underlying mechanisms. Isolated rat Leydig ceils were treated with annexin A5. Testosterone produc...This study was to investigate the effect of annexin A5 on testosterone secretion from primary rat Leydig cells and the underlying mechanisms. Isolated rat Leydig ceils were treated with annexin A5. Testosterone production was detected by chemiluminescence assay. The protein and mRNA of Steroidogenic acute regulatory （STAR）, P450scc, 3β-hydroxysteroid dehydrogenase （3β-HSD）, 17β-hydroxysteroid dehydrogenase （17β-HSD）, and 17β-hydroxylase were examined by Western blotting and semi-quantitative RT-PCR, respectively. Annexin A5 significantly stimulated testosterone secretion from rat Leydig cells in dose- and time-dependent manners and increased mRNA and protein expression of STAR, P450scc, 3β-HSD, and 17β-HSD but not 17α-hydroxylase. Annexin A5 knockdown by siRNA significantly decreased the level of testosterone and protein expression of P450scc, 3β-HSD, and 17β-HSD. The significant activation of ERK1/2 signaling was observed at 5, 10, and 30 min after annexin A5 treatment. After the pretreatment of Leydig cells with ERK inhibitor PD98059 （50 μmol l^-1） for 20 min, the effects of annexin A5 on promoting testosterone secretion and increasing the expression of P450scc, 3β-HSD, and 17β-HSD were completely abrogated （P 〈 0.05）. Thus, ERK1/2 signaling is involved in the roles of annexin A5 in mediating testosterone production and the expression of P450scc, 3β-HSD, and 17β-HSD in Leydig cells.展开更多
Annexin A5 is a Ca2?-dependent phospholipidbinding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we ...Annexin A5 is a Ca2?-dependent phospholipidbinding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tissues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to determine the effects of annexin A5 upregulation on the cell morphology, proliferation and metastasis potential in vitro.The effects of annexin A5 on NCI-H520 cells were tested by crystal violet staining, CCK-8 assay, scratch wound assay, and Transwell assay. The expressions of Akt,PCNA, vimentin, and E-cadherin were examined by Western blot assay. In this study, we demonstrated that annexin A5 is expressed at lower levels in tumor tissues compared with normal tissues. Additionally, the upregulation of this protein may inhibit the proliferation, migration, and invasion abilities of NCI-H520 cells in vitro. The transfected cells were arrested in the G1/S phase of the cell cycle, and the expression levels of Akt, PCNA and Vimentin were downregulated, while E-cadherin was upregulated.展开更多
文摘AIM To investigate the expression of annexin A5 in serum and tumor tissue of patients with colon cancer and to analyze its clinical significance.METHODS Ninety-three patients with colon cancer treated at our hospital between February 2013 and March 2016 were included in an observation group, and 40 healthy individuals were included in a control group. Enzyme-linked immunosorbent assay was performed to determine the serum level of annexin A5, while immunohistochemistry was performed to determine the expression of annexin A5 in cancer tissues.RESULTS The serum level of annexin A5 was 0.184 ± 0.043 ng/m L in the observation group, which was significantly higher than that in the control group(P < 0.05). Annexin A5 expression was detected in 79.31% of the patients with lymph node metastasis, which was significantly higher than that in patients without lymph node metastasis(P < 0.05). Moreover, annexin A5 expression was detected in 86.96% of the patients with stage Ⅲ to Ⅳ disease, which was significantly higher than that in patients with stage Ⅰ to Ⅱ disease(P < 0.05). The serum level of annexin A5 was 0.215 ± 0.044 ng/m L in patients whose tumors were positive for annexin A5 expression, which was significantly higher than that in patients whose tumors were negative for annexin A5 expression(P < 0.05). The serum level of annexin A5 was correlated with annexin A5 expression in colon cancer tissues(r= 0.312, P < 0.05). When a cutoff value of > 0.148 ng/m L for serum level of annexin A5 was used in the diagnosis of colon cancer, the sensitivity was 83.90%, and the specificity was 57.50%.CONCLUSION For patients with colon cancer, annexin A5 expression in cancer tissues is related to lymph node metastasis and tumor grade. Serum level of annexin A5 is related to annexin A5 expression in cancer tissues and is of diagnostic relevance.
文摘This study was to investigate the effect of annexin A5 on testosterone secretion from primary rat Leydig cells and the underlying mechanisms. Isolated rat Leydig ceils were treated with annexin A5. Testosterone production was detected by chemiluminescence assay. The protein and mRNA of Steroidogenic acute regulatory （STAR）, P450scc, 3β-hydroxysteroid dehydrogenase （3β-HSD）, 17β-hydroxysteroid dehydrogenase （17β-HSD）, and 17β-hydroxylase were examined by Western blotting and semi-quantitative RT-PCR, respectively. Annexin A5 significantly stimulated testosterone secretion from rat Leydig cells in dose- and time-dependent manners and increased mRNA and protein expression of STAR, P450scc, 3β-HSD, and 17β-HSD but not 17α-hydroxylase. Annexin A5 knockdown by siRNA significantly decreased the level of testosterone and protein expression of P450scc, 3β-HSD, and 17β-HSD. The significant activation of ERK1/2 signaling was observed at 5, 10, and 30 min after annexin A5 treatment. After the pretreatment of Leydig cells with ERK inhibitor PD98059 （50 μmol l^-1） for 20 min, the effects of annexin A5 on promoting testosterone secretion and increasing the expression of P450scc, 3β-HSD, and 17β-HSD were completely abrogated （P 〈 0.05）. Thus, ERK1/2 signaling is involved in the roles of annexin A5 in mediating testosterone production and the expression of P450scc, 3β-HSD, and 17β-HSD in Leydig cells.
基金supported by the National Basic Research Program of China (2012CB967003)National Natural Science Foundation of China (81272225)+2 种基金the Research Fund for the Docoral Program of Higher Education of China (20132106110006)the Science Foundation of Liaoning Province Education Administration (L2013350)Dalian Science Foundation (2011E12SF036).
文摘Annexin A5 is a Ca2?-dependent phospholipidbinding protein and protein kinase C inhibitory protein. It has a potential role in cellular signal transduction, inflammation, growth and differentiation. In this study, we evaluated the expression of this protein in lung tumor tissues and subsequently established a NCI-H520 cell line that stably expresses the wild-type ANXA5 gene to determine the effects of annexin A5 upregulation on the cell morphology, proliferation and metastasis potential in vitro.The effects of annexin A5 on NCI-H520 cells were tested by crystal violet staining, CCK-8 assay, scratch wound assay, and Transwell assay. The expressions of Akt,PCNA, vimentin, and E-cadherin were examined by Western blot assay. In this study, we demonstrated that annexin A5 is expressed at lower levels in tumor tissues compared with normal tissues. Additionally, the upregulation of this protein may inhibit the proliferation, migration, and invasion abilities of NCI-H520 cells in vitro. The transfected cells were arrested in the G1/S phase of the cell cycle, and the expression levels of Akt, PCNA and Vimentin were downregulated, while E-cadherin was upregulated.
