ABSTRACT
Objective:To investigate effect and mechanism of mangiferin on regulation of M2-type macrophage polarization tar-geting MMP9 in pancreatic cancer.Methods:In vivo,therapeutic effect of mangiferin on pancreatic cancer was evaluated by drawing tumor growth curves and immunohistochemical staining.M2-type macrophages expression in pancreatic cancer was detected by immu-nofluorescence and ELISA.Effects of mangiferin on expression of MMP9 and downstream M2 macrophage polarization-related signaling pathways were detected by immunofluorescence,ELISA,Western blot and qRT-PCR.In vitro,MTT assay was utilized to detect effect of mangiferin on M2-type macrophage and therapeutic effect of mangiferin on pancreatic cancer.ELISA was used to detect effect of mangiferin on M2-type polarized macrophages.Effects of mangiferin on expression of MMP9 and its downstream signalling pathway were detected by immunofluorescence and Western blot.Results:Mangiferin had potential to inhibit growth of pancreatic cancer in mice pancreatic model,and could prevent expression of M2-polarized macrophages in pancreatic cancer in addition.At the same time,mangiferin could inhibit expression of MMP9 and downstream M2 macrophage polarization related signaling pathways in pancreatic cancer.Mangiferin inhibited proliferation of pancreatic cancer cells in a M2 type polarized macrophage-pancreas cancer cell co-culture model,inhibited macrophage M2 polarization,at the same time,expression of MMP9 and downstream M2 macrophage polarization related signaling pathway was inhibited.Conclusion:Mangiferin can inhibit macrophage M2 polarization by inhibiting MMP9 and its downstream signaling pathway,and play a role in pancreatic cancer therapy.
ABSTRACT
OBJECTIVE:To investigate clinical significance of programmed cell death 5 (PDCD5) protein in serum of pa-tients with lung cancer. METHODS:80 lung cancer inpatients were selected from the First Affiliated Hospital of Shihezi University School of Medicine(hereinafter referred to asour hospital)as lung cancer group;60 healthy volunteers were selected from our hospital at the same period as normal group. ELISA was used to test the expression of PDCD5 protein,and the relationship of PDCD5 protein with clinical pathological features of lung cancer patients were analyzed. RESULTS:The expression of PDCD5 pro-tein in normal group was significantly higher than lung cancer group,with statistical significance (P0.05);it was de-creased as the decrease of tumor differentiation degree,with statistical significance(P<0.05). The expression of PDCD5 protein in patients with carcinoembryonic antigen(CEA)<5.6μmol/L was significantly higher than those with CEA≥5.6μmol/L;the expres-sion of PDCD5 protein in patients with cytokeratin 19 soluble fragment (CYFRA21-1)<5.6 μmol/L was significantly higher than those with CYFRA21-1≥5.6 μmol/L,with statistical significance(P<0.05). The expression of PDCD5 protein in patients with Ⅰ-Ⅱ stage lung cancer was significantly higher than Ⅲ-Ⅳ stage lung cancer patients;the expression of PDCD5 protein in patients without distant metastasis was significantly higher than those with distant metastasis. The expression of PDCD5 protein was in de-creasing as the increase of the number of metastasis site,with statistical significance(P<0.05). CONCLUSIONS:PDCD5 protein in serum of patients with lung cancer shows low expression level,which is related to tumor differentiation degree,tumor marker level as CEA and CYFRA21-1,tumor stage and distant metastasis,etc. The detection of PDCD5 protein may contribute to clinical diagnosis of lung cancer.
ABSTRACT
Objective To explore the clinical value of expression levels of serum COX-2 in patients with advanced NSCLC before and after EGFR-TKI treatment. Methods The serum was collected from 58 cases. Before and after targeted therapy , the serum COX-2 level was examined by ELISA. Meanwhile , CT scan was exercised to evaluate the treatment. Follow-up interview was done. The relationship among the change in expression level of serum COX-2 , efficacy and PFS was analyzed. Results The serum COX-2 level significantly decreased in the response group (t = 11.258, P = 0.000) and increased in the PD group (t = -7.759, P =0.000) after EGFR-TKI treatment, and not significantly changed in the SD group (t = 1.424, P = 0.170). Before treatment, the baseline serum COX-2 level in the response group was significantly higher than that in the SD group and the PD group (F = 20.852, P = 0.000 ). Before the targeted therapy, the higher the level of serum COX-2 was, the longer PFS patients would enjoy. Conclusion Detection of the serum COX-2 contributes to the judgment of therapeutic effect of EGFR-TKI and can be used as a prediction of EGFR-TKI drugs outcomes for patients with advanced NSCLC.
ABSTRACT
<p><b>OBJECTIVE</b>To study the prevention of colorectal cancer liver metastasis by adenoviral transduction of the endostatin gene.</p><p><b>METHODS</b>The recombinant adenovirus expressing endostatin was constructed. Its biological activities were surveyed in vitro, as determined in human umbilicus vein endothelium cell (HUVEC) proliferation inhibition, and in vivo, by reduction of liver metastasis.</p><p><b>RESULTS</b>HUVEC proliferation was obviously inhibited by the infecting supernatant of recombinant adenovirus. Persistent high serum levels of endostatin in peripheral blood, especially in the liver vein were observed. The production of liver metastasis was intervened.</p><p><b>CONCLUSIONS</b>The single injection in the vein of the recombinant adenovirus realizes the high effective and stable expression of endostatin in general body and liver, which brings about the ideal prevention of liver metastasis.</p>
Subject(s)
Animals , Mice , Adenoviridae , Genetics , Cell Division , Collagen , Genetics , Therapeutic Uses , Colorectal Neoplasms , Pathology , Disease Models, Animal , Endostatins , Endothelium, Vascular , Pathology , Genetic Therapy , Genetic Vectors , Liver Neoplasms , Mice, Inbred BALB C , Neoplasm Metastasis , Neoplasm Transplantation , Peptide Fragments , Genetics , Therapeutic Uses , Transduction, GeneticABSTRACT
Objective To study the significance of monitoring postoperative hematogenous micrometastasis of colorectal cancer. Methods The micrometastatic cancer cells in peripheral blood and bone marrow of the perioperative patients were investigated by CK20 mRNA RT-PCR. Results The positive rates(16.3%) of hematogenous dissemination without relapse or metastasis after operation were significantly lower than that(88.9%) in patients with postoperative relapse or metastasis. There were four types of hematogenous dissemination. (1) Postoperative temporary negatives.(2)Consistant positives. (3) CK-20 turned positive postoperatively. (4) Consistant negatives. All the 6 patients that died had positive CK-20 preoperatively. Conclusions The hematogenous dissemination of colorectal cancer plays an important role in postoperative relapse. The dynamic monitoring of CK-20 predicts hematogenous dissemination of colorectal cancer.
ABSTRACT
ObjectiveTo explore the recurrence inhibition of colorectal cancer by adenoviral transducted endostatin gene. Methods The recombinant adenovirus expressing endostatin was constructed. Its biological activities were observed. The levels of endostatin in mice peripheral blood, tumor local recurrence and tumor cell apotosis were analyzed after the endostatin gene transduction by adenovirus. Results The infecting supernatant of recombinant adenovirus significantly inhibited HUVEC proliferation. After the injection of the recombinant adenovirus, persistent high serum levels of endostatin in peripheral blood was observed, local recurrence rate decreased, and apotosis of recurrence tumor cells increased.Conclusions The intraveneously injection of recombinant adenovirus mediated endostatin gene produces high concentration and stable expression of endostatin,which effects prevention of local recurrence after surgical resection of colorectal cancer.