OBJECTIVE To investigate whether CXCL12 and its receptor, CXCR7, play a role in lung cancer invasion and metastasis. METHODS Western blot and immunocytochemistry were used to detect CXCR7 protein expression in 8 lung ...OBJECTIVE To investigate whether CXCL12 and its receptor, CXCR7, play a role in lung cancer invasion and metastasis. METHODS Western blot and immunocytochemistry were used to detect CXCR7 protein expression in 8 lung cancer cell lines, EKVX, HOP62, HOP92, NCI-H23, NCI-H226, NCI- H322M, NCI-H446, and A549, and cell migration experiment was conducted to observe mobility of the lung cancer cells. The concentration of intracellular calcium in cytoplasm was measured under the fluorescence microscopy. RESULTS CXCR7 protein was positively expressed in the 8 lung cancer cell lines EKVX, HOP62, HOP92, NCI-H23, NCI-H226, NCI- H322M, NCI-H446, and A549. Following CXCL12 stimulation, obvious pseudopodia of lung cancer cells was observed under the microscope. The cell migration experiment showed that after incubation with CXCL12, the number of EKVX cells, which passed through the polycarbonate microporous filter membranes increased to a great extent. This phenomenon can be reversed by CXCR7-siRNA. After CXCL12 incubation, the intracellular Ca2＋ level in the EKVX cells was increased to a great extent. CONCLUSION Chemokine CXCL12 facilitates the migration of lung cancer cells by changing the concentration of intracellular Ca2＋. The CXCL12-CXCR7 axis may play an important role in lung cancer invasion and metastasis. It could be a potential target for lung cancer therapy and an effective way to prevent recurrence and metastasis of lung cancer.展开更多
Background Heart failure due to ischemic heart disease is still a major health problem. Myocardium regeneration emerges as a novel therapeutic method for treating myocardial infarction （MI）. However, it is affected ...Background Heart failure due to ischemic heart disease is still a major health problem. Myocardium regeneration emerges as a novel therapeutic method for treating myocardial infarction （MI）. However, it is affected by many factors. The present study was aimed to investigate the effect of chemokine stromal cell-derived factor 1 （SDF-1）/CXCL12 on mesenchymal stem cells （MSCs） homing to injured myocardium in a rat myocardial infarction model. Methods A rat myocardial infarction model was established by permanent left anterior descending branch ligation. Mesenchymal stem cells from donor rats were cultured in IMDM and labeled with bromodeoxyuridine. The rats were divided into two groups. SDF-1 expression was measured by in situ hybridization and immunohistochemistry in the sham operated or infarcted hearts at 1, 2, 4, 7, 14 and 28 days post operation in the SDF-1 detection group. The rats in the intervention groups were injected with SDF-1, anti-SDF-1 antibody or saline 4 days after myocardial infarction. Then, a total of 5×10^6 cells in 2.5 ml of phosphate-buffered saline were injected through the tail vein. The number of the labeled MSCs in the infarcted hearts was counted on the 3rd day post injection. Cardiac function and blood vessel density were assessed on the 28th day post injection. Results Self-generating SDF-1 expression was increased at the first day post MI, peaked at the 7th day and decreased thereafter while it remained unchanged in sham operated hearts. The MSCs enrichment in the host hearts were more abundant in the MI groups than in the non-MI group （P=0.000）; the MSCs enrichment in the host hearts were more abundant in the SDF-1 injected group than in the anti-SDF-1 antibody and saline injected groups （P = 0.000）. Cardiac function was improved more in the SDF-1 injected group than in the anti-SDF-1 antibody and saline injected groups （P = 0.000）. Neovascularization in the SDF-1 injected group increased significantly compared to the other groups （P= 0.000）. Conclusion Myocardial SDF-1 expression was increased only in the early phase post MI. SDF-1 may enhance MSCs homing to the injured heart and improve cardiac function by promoting neovascularization. Chin Med J 2009; 122（2）： 183-187展开更多
文摘OBJECTIVE To investigate whether CXCL12 and its receptor, CXCR7, play a role in lung cancer invasion and metastasis. METHODS Western blot and immunocytochemistry were used to detect CXCR7 protein expression in 8 lung cancer cell lines, EKVX, HOP62, HOP92, NCI-H23, NCI-H226, NCI- H322M, NCI-H446, and A549, and cell migration experiment was conducted to observe mobility of the lung cancer cells. The concentration of intracellular calcium in cytoplasm was measured under the fluorescence microscopy. RESULTS CXCR7 protein was positively expressed in the 8 lung cancer cell lines EKVX, HOP62, HOP92, NCI-H23, NCI-H226, NCI- H322M, NCI-H446, and A549. Following CXCL12 stimulation, obvious pseudopodia of lung cancer cells was observed under the microscope. The cell migration experiment showed that after incubation with CXCL12, the number of EKVX cells, which passed through the polycarbonate microporous filter membranes increased to a great extent. This phenomenon can be reversed by CXCR7-siRNA. After CXCL12 incubation, the intracellular Ca2＋ level in the EKVX cells was increased to a great extent. CONCLUSION Chemokine CXCL12 facilitates the migration of lung cancer cells by changing the concentration of intracellular Ca2＋. The CXCL12-CXCR7 axis may play an important role in lung cancer invasion and metastasis. It could be a potential target for lung cancer therapy and an effective way to prevent recurrence and metastasis of lung cancer.
文摘Background Heart failure due to ischemic heart disease is still a major health problem. Myocardium regeneration emerges as a novel therapeutic method for treating myocardial infarction （MI）. However, it is affected by many factors. The present study was aimed to investigate the effect of chemokine stromal cell-derived factor 1 （SDF-1）/CXCL12 on mesenchymal stem cells （MSCs） homing to injured myocardium in a rat myocardial infarction model. Methods A rat myocardial infarction model was established by permanent left anterior descending branch ligation. Mesenchymal stem cells from donor rats were cultured in IMDM and labeled with bromodeoxyuridine. The rats were divided into two groups. SDF-1 expression was measured by in situ hybridization and immunohistochemistry in the sham operated or infarcted hearts at 1, 2, 4, 7, 14 and 28 days post operation in the SDF-1 detection group. The rats in the intervention groups were injected with SDF-1, anti-SDF-1 antibody or saline 4 days after myocardial infarction. Then, a total of 5×10^6 cells in 2.5 ml of phosphate-buffered saline were injected through the tail vein. The number of the labeled MSCs in the infarcted hearts was counted on the 3rd day post injection. Cardiac function and blood vessel density were assessed on the 28th day post injection. Results Self-generating SDF-1 expression was increased at the first day post MI, peaked at the 7th day and decreased thereafter while it remained unchanged in sham operated hearts. The MSCs enrichment in the host hearts were more abundant in the MI groups than in the non-MI group （P=0.000）; the MSCs enrichment in the host hearts were more abundant in the SDF-1 injected group than in the anti-SDF-1 antibody and saline injected groups （P = 0.000）. Cardiac function was improved more in the SDF-1 injected group than in the anti-SDF-1 antibody and saline injected groups （P = 0.000）. Neovascularization in the SDF-1 injected group increased significantly compared to the other groups （P= 0.000）. Conclusion Myocardial SDF-1 expression was increased only in the early phase post MI. SDF-1 may enhance MSCs homing to the injured heart and improve cardiac function by promoting neovascularization. Chin Med J 2009; 122（2）： 183-187
