ABSTRACT
Objective To investigate the preventive and inhibitory effects of tumor cell lysate(TCL) combined with IL-2 on melanoma and the potential immune mechanism. Methods The B16F10 melanoma TCL cell were prepared using an ultrasonic disruptor. Twenty-four C57BL/6 mice were randomly divided into four groups which were immunized with PBS, IL-2, TCL and TCL+IL-2 for three weeks, and contra lateral tumors were implanted in the fourth week. We observed onset time of tumor and tumor size, collected peripheral blood continuously and monitored the expression of CD4+T and CD8+T cell subsets dynamically by flow cytometry. Spleen and tumor tissues of mice were also tested for CD4+T and CD8+T cell subsets by flow cytometry and immunohistochemistry, respectively. Results The preventive immunization of the TCL+IL-2 group significantly delayed the onset time of tumor (P=0.034); moreover, the tumor volume (P=0.023) and tumor weight (P=0.0015) were also significantly smaller than those in the control group. The expression of CD8+T cell subsets in the TCL+IL-2 group and the TCL-only group were significantly higher than that in the control group (P=0.0016, P=0.012). However, the CD4+T cell subsets of the TCL+IL-2 group decreased after tumor implantation, compared with the control group (P=0.0089). The expression of CD4+T and CD8+T cell subsets in spleen and tumor tissues were as same as those in peripheral blood. Conclusion The tumor vaccine of TCL combined with IL-2 could prevent the occurrence of melanoma in mouse and effectively inhibit tumor growth by activating CD8+T cells.
ABSTRACT
Objective:To discuss the diagnostic value of miR-26a/b and relationship of this microRNA with clinicopathological features in patients with gastric cancer. Methods:The expression of serum miR-26a/b was detected in 121 patients with gastric cancer and 116 healthy controls using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The relationship of miR-26a/b and clinicopathological parameters of patients were analyzed. The receiver operating curve (ROC) was constructed to in vestigate the value of miR-26a/b in the diagnosis of gastric cancer. Results:The relative expression levels of serum miR-26a and miR-26b in patients with gastric cancer were lower than those in the control group (1.60±1.02 vs. 5.35±0.44;1.44±0.71 vs. 5.35±0.71;P<0.05). The relative expression level of miR-26a/b correlated with TNM stage, and the relative expression level of miR-26a also correlated with invasion depth and lymph node metastasis (P<0.05), but not with sex, age, tumor size, or histological type (P>0.05). The area under the ROC curve of miR-26a was 0.828 (95％CI:0.776～0.881), with sensitivity of 73.3％and specificity of 81.0％, while the area under the ROC curve of miR-26b was 0.853 (95％CI:0. 801～0.906), with sensitivity of 68.1％and specificity of 99.2％. Conclusion:The expression of miR-26a/b significantly reduced in patients with gastric cancer, and its expression level correlated with the clinical stage, invasion depth, and lymph node metastasis. MiR-26a/b has potential diagnostic value for gastric cancer.
ABSTRACT
It has been found that diabetes is closely correlated with the occurrence of colorectal cancer, as an independent risk factor for colorectal cancer. In order to prolong the survival time and to improve the quality of life of colorectal cancer patients with diabetes, many studies have explored the influence of diabetes on the prognosis of patients with colorectal cancer in recent years. Some studies have confirmed diabetes is related to the prognosis of colorectal cancer, while other studies have suggested that diabetes is not correlated with the prognosis of colorectal cancer. Until now, it is still unclear whether the presence of diabetes has impact on the prognosis of colorectal cancer. Therefore, this problem has become one of the hot topics in cancer research field recently. This article reviews the research progress in the relationship between diabetes and the prognosis of patients with colorectal cancer.
ABSTRACT
Objective:To investigate the role and mechanism of miR-143 in the proliferation and migration of gastric cancer (GC) cells. Methods:Western blot was performed to detect the expression level of avian erythroblastosis oncogene B-3 (ERBB3) in GC tissues, paired non-cancerous tissues, and SGC7901 GC cells. RT-qPCR was conducted to determine the mRNA and miR-143 of ERBB3 quantita-tively. Bioinformatics tools were used to predict the target gene of miR-143. Luciferase reporter assay was carried out to confirm the predicted target gene. Transwell and EdU assays were applied to observe the migration and proliferation of SGC7901 GC cells transfect-ed with miR-143 mimics/inhibitor/NC mimics/inhibitor. Results:Compared with the expression levels of ERBB3 and miR-143 in the paired non-cancerous tissues, the expression level of ERBB3 was upregulated and the expression level of miR-143 was downregulated in GC tissues. In the prediction of the potential target gene, miR-143 could bind to a specific sequence of the 3′-untranslated regions (UTR) of the mRNA of ERBB3. This finding was supported by luciferase reporter assay results. In vitro, ERBB3 protein expression and cell migration and proliferation were suppressed significantly in the SGC7901 cells transfected with miR-143 mimics. By contrast, these processes were remarkably enhanced when the cells were transfected with miR-143 inhibitor. Conclusion:miR-143 can suppress the migration and proliferation of GC cells by downregulating the expression of ERBB3.