AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of...AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of β-catenin expression with cyclinDl, c-myc and MMP-7 expression. METHODS: Using immunohistochemistry,we examined the expression of β-catenin, cyclinD1,c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreatic intraepithelial neoplasia (PanIN) and 10 normal pancreases, respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells. RESULTS: In 10 cases of normal pancreatic tissues, epithelial cells showed equally strong membranous expression of β-catenin protein at the cell-cell boundaries, but the expression of cyclinDl, c-myc and MMP-7 was negative. The expression of β-catenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%), 6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12 and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation. The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size, metastasis and one-year survival rate of the pancreatic cancer. The expression of c-myc was not correlated with size, extent of differentiation, metastasis and 1-year survival rate, but closely with cell proliferation of pancreatic cancer. The overexpression of MMP-7 was significantly associated with metastasis and 1-year survival rate of pancreatic cancer,but not with size, extent of differentiation and cell proliferation.There was a highly significant positive association between abnormal expression of β-catenin and overexpression of cyclinD1, c-myc and MMP-7 not o展开更多
AIM： To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion.METHODS： Fifty-four SD rats were randomly divided into ischemic preconditioning gro...AIM： To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion.METHODS： Fifty-four SD rats were randomly divided into ischemic preconditioning group （IP）, ischemia/ reperfusion group （IR） and sham operation group （SO）. The IP and IR groups were further divided into four sub-groups （n = 6）. Sham operation group （SO） served as the control group （n = 6）. A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. Alter 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinD1 mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS： Compared with IR group, IP group showed a significantly lower ALT level in 1h to 4h sub-groups （P 〈 0.05）. Proliferation index（PI） indicated by the S-phase and G2/M-phase ratio [（S＋G2/M）/（G0/G1＋S＋G2/M）] was significantly increased in IP group at 0 and 1 h （26.44 ± 7.60% vs 18.56 ± 6.40%,41.87 ± 7.27% vs 20.25 ± 6.70%, P 〈 0.05）. Meanwhile, cyclinD1 protein expression could be detected in IP group. But in IR group, cyclinD1 protein expression occurred 2 h alter reperfusion. The expression of cyclinD1 mRNA increased significantly in IP group at 0 and 1h （0.568 ± 0.112 vs 0.274 ± 0.069, 0.762 ± 0.164 vs 0.348 ± 0.093,P 〈 0.05）.CONCLUSION： Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion.展开更多
基金Supported by the Foundation of Shandong Education Committee,No. 03K02
文摘AIM:To investigate whether abnormal expression of β-catenin in conjunction with overexpression of cyclinD1, c-myc and matrix metalloproteinase-7 (MMP-7) correlated with the carcinogenesis, metastasis and prognosis of pancreatic cancer, and to analyze the relationship of β-catenin expression with cyclinDl, c-myc and MMP-7 expression. METHODS: Using immunohistochemistry,we examined the expression of β-catenin, cyclinD1,c-myc and MMP-7 in 47 pancreatic adenocarcinoma tissues, 12 pancreatic intraepithelial neoplasia (PanIN) and 10 normal pancreases, respectively. Proliferation cell nuclear antigen was also tested as the index of proliferative activity of pancreatic cancer cells. RESULTS: In 10 cases of normal pancreatic tissues, epithelial cells showed equally strong membranous expression of β-catenin protein at the cell-cell boundaries, but the expression of cyclinDl, c-myc and MMP-7 was negative. The expression of β-catenin, cyclinD1, c-myc and MMP-7 in PanIN and pancreatic adenocarcinoma tissues had no significant difference [6/12 and 32/47 (68.1%), 6/12 and 35/47 (74.5%), 5/12 and 33/47 (70.2%), 7/12 and 30/47 (63.8%), respectively]. The abnormal expression of β-catenin was significantly correlated to metastasis and one-year survival rate of pancreatic cancer, but had no relation with size, differentiation and cell proliferation. The expression of cyclinD1 was correlated with cell proliferation and extent of differentiation, but not with size, metastasis and one-year survival rate of the pancreatic cancer. The expression of c-myc was not correlated with size, extent of differentiation, metastasis and 1-year survival rate, but closely with cell proliferation of pancreatic cancer. The overexpression of MMP-7 was significantly associated with metastasis and 1-year survival rate of pancreatic cancer,but not with size, extent of differentiation and cell proliferation.There was a highly significant positive association between abnormal expression of β-catenin and overexpression of cyclinD1, c-myc and MMP-7 not o
基金Supported by Youth Foundation of Health Bureau of Fujian Province, No. 2003-1-19
文摘AIM： To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion.METHODS： Fifty-four SD rats were randomly divided into ischemic preconditioning group （IP）, ischemia/ reperfusion group （IR） and sham operation group （SO）. The IP and IR groups were further divided into four sub-groups （n = 6）. Sham operation group （SO） served as the control group （n = 6）. A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. Alter 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinD1 mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS： Compared with IR group, IP group showed a significantly lower ALT level in 1h to 4h sub-groups （P 〈 0.05）. Proliferation index（PI） indicated by the S-phase and G2/M-phase ratio [（S＋G2/M）/（G0/G1＋S＋G2/M）] was significantly increased in IP group at 0 and 1 h （26.44 ± 7.60% vs 18.56 ± 6.40%,41.87 ± 7.27% vs 20.25 ± 6.70%, P 〈 0.05）. Meanwhile, cyclinD1 protein expression could be detected in IP group. But in IR group, cyclinD1 protein expression occurred 2 h alter reperfusion. The expression of cyclinD1 mRNA increased significantly in IP group at 0 and 1h （0.568 ± 0.112 vs 0.274 ± 0.069, 0.762 ± 0.164 vs 0.348 ± 0.093,P 〈 0.05）.CONCLUSION： Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion.
