Objective:To investigate the roles of secretory phosphoprotein 1(SPP1)in the progression of colorectal cancer(CRC)and the underlying mechanism.Methods:Gene Expression Profiling Interactive Analysis(GEPIA)database was used to obtain the expression of SPP1 gene in CRC.Immunohistochemistry analysis and Western blotting were used to detect the expression of SPP1 in distal normal colorectal tissues,adjacent tissues,CRC tissues,normal colorectal cell lines and CRC cell lines.The cell viability,colony formation,migration and invasion of CRC cells as well as the activation of AKT/glycogen synthase kinase 3β(GSK3β)signaling pathway and the expression of epithelial-mesenchymal transition(EMT)-related proteins in HT-29 cells and HCT-116 cells were detected by CCK-8 assay,colony formation assay,trranswell assay and Western blotting after SPP1 knockdown in vitro through lentiviral infection carrying shRNA against SPP1 gene.Tumor formation assay was used to detect the effect of SPP1 knockdown on the growth and lung metastasis of transplanted HT-29 tumor in vivo.Results:SPP1 expression was significantly increased in CRC tissues and cell lines(P<0.001)and was associated with poor prognosis of CRC patients according to GEPIA database analysis.The expression of SPP1 protein was significantly upregulated in CRC tissues and cells(P<0.001).After knockdown of SPP1 expression,the cell viability,colony formation,migration and invasion of CRC cells were significantly decreased(P<0.001),the expression of phosphorylated AKT(phospho-AKT,p-AKT),phosphorylated GSK3β(phospho-GSK3β,p-GSK3β),Snail and Vementin were significantly decreased(P<0.001),while E-cadherin expression was significantly increased(P<0.001).Knockdown of SPP1 expression inhibited the growth and lung metastasis of HT-29 cell tumor xenografts in mice.Conclusion:SPP1 knockdown can inhibit the proliferation,migration and invasion of CRC cells,which may be related to the reduction of AKT/GSK3β signaling activity.

Objective:To investigate the roles of secretory phosphoprotein 1(SPP1)in the progression of colorectal cancer(CRC)and the underlying mechanism.Methods:Gene Expression Profiling Interactive Analysis(GEPIA)database was used to obtain the expression of SPP1 gene in CRC.Immunohistochemistry analysis and Western blotting were used to detect the expression of SPP1 in distal normal colorectal tissues,adjacent tissues,CRC tissues,normal colorectal cell lines and CRC cell lines.The cell viability,colony formation,migration and invasion of CRC cells as well as the activation of AKT/glycogen synthase kinase 3β(GSK3β)signaling pathway and the expression of epithelial-mesenchymal transition(EMT)-related proteins in HT-29 cells and HCT-116 cells were detected by CCK-8 assay,colony formation assay,trranswell assay and Western blotting after SPP1 knockdown in vitro through lentiviral infection carrying shRNA against SPP1 gene.Tumor formation assay was used to detect the effect of SPP1 knockdown on the growth and lung metastasis of transplanted HT-29 tumor in vivo.Results:SPP1 expression was significantly increased in CRC tissues and cell lines(P<0.001)and was associated with poor prognosis of CRC patients according to GEPIA database analysis.The expression of SPP1 protein was significantly upregulated in CRC tissues and cells(P<0.001).After knockdown of SPP1 expression,the cell viability,colony formation,migration and invasion of CRC cells were significantly decreased(P<0.001),the expression of phosphorylated AKT(phospho-AKT,p-AKT),phosphorylated GSK3β(phospho-GSK3β,p-GSK3β),Snail and Vementin were significantly decreased(P<0.001),while E-cadherin expression was significantly increased(P<0.001).Knockdown of SPP1 expression inhibited the growth and lung metastasis of HT-29 cell tumor xenografts in mice.Conclusion:SPP1 knockdown can inhibit the proliferation,migration and invasion of CRC cells,which may be related to the reduction of AKT/GSK3β signaling activity.

Objective:To investigate the effect of chemotherapy combined with sorafenib on the prognosis of FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukemia and to find a more effective treatment.Methods:The clinical data of 60 patients who were newly diagnosed with acute myeloid leukemia and who received treatment in The Second Affiliated Hospital of Qiqihar Medical University from January 2015 to January 2017 were retrospectively analyzed. The patients were divided into three groups according to whether they were positive for FLT3-ITD and the treatment method they used. The observation group (FLT3-ITD-positive, n = 19) were treated with sorafenib based on routine chemotherapy. The control group 1 (FLT3-ITD-positive, n = 21) was treated only with routine chemotherapy. The control group 2 (FLT3-ITD-negative, n = 20) was treated only with routine chemotherapy. After the first and fourth courses of treatment, clinical efficacy was compared among the three groups. Results:After the first course of treatment, the complete remission rate in control group 2 was 50.0% (10/20), which was significantly higher than 15.8% (3/19) in the observation group and 4.8% (1/21) in the control group 1 ( H = 13.39, P < 0.05). After the fourth course of treatment, the complete remission rate in the observation group, control group 2, and control group 1 was 63.2% (12/19), 60.0% (12/20), and 4.8% (1/21), respectively, and the differences were statistically significant ( H = 19.21, P < 0.05). Four-year follow-up results showed that the median survival time in the observation group, control group 1, and control group 2 was 36.63, 24.15, and 45.00 months respectively. The event-free survival in the observation group, control group 1, and control group 2 was 18.00, 9.82, and 24.90 months, respectively. The median survival time and the event-free survival in the control group 2 were significantly longer than those in the observation group and control group 1 ( χ2 = 19.93, 23.04, both P < 0.001). Conclusion:Chemotherapy combined with sorafenib for treating newly-diagnosed FLT3-ITD-positive acute myeloid leukemia can provide comprehensive benefits and have advantages for survival over chemotherapy without sorafenib and chemotherapy alone.

Objective To investigate the changes of estrogen receptor expression in mast cells of bronchial mucosa from female asthmatic patients.Methods 12 cases of female asthmatic patients and 9 cases of control female patients were enrolled in this study.The bronchial mucosa was obtained from the third grade bronchial by fiexible bronchofiberscope.Mast cells were marked by anti-mast cell tryptase monoclonal antibody,the expression of estrogen receptor(ER)were detected by anti-human estrogen receptor(ER)monoclonal antibodies.Results Mast cells and estrogen receptor positive cells of bronchial mucosa in female asthmatic patients were significantly higher than that in control group(P＜0.01).Coincident with the known features of bronchial asthma,the cells positive for estrogen receptor were morphologically similar to the mast cells.The cells stained for estrogen receptors by dual immunostaining coincided exactly with cells labeled as mast cells.Conclusion The result suggested the estrogen may be involved in the pathogenesis of female asthmatic patient through the changes of estrogen receptor expression in mast cells of bronchial mucosa.