Objective To explore the influence on cyclin and cyclin-dependent kinase inhibitor of cell cycle of Kasumi-1 cell-derived from t(8;21)/AML treated with histone deacetylase(HDAC)inhibitor valproic acid(VPA).Methods RT-PCR assay was applied to detect mRNA expression of regulation factor of cell cycle of Kasumi-1 cell with VPA at different concentration and different time. Results VPA could down-regulate mRNA expression of cyclinD1,cyclinE1 and cyclinB1,and up-regulate mRNA expression of p21 WAF1/CIP1 with no obvious variation of mRNA level of p27KIP1. Condusion VPA could regulate cell cycle through the regulation of cyclins and cyclin-dependent kinase,arresting Kasumi-1 cell at G0/G1 phase.

Pulse diagnosis system of traditional Chinese medicine is a complicated nonlinear macrosystem.Directed by complexity science theory,and introduced with idea of complex-simple-complex,the pulse diagnosis message is multidimensionally extracted,analyzed with reduced integration,and integrated with upgrade stage and dimension,according to four kinds of attributes "the Position,the Rate,the Shape,the Force".After the digitization,the new kind of pulses diagnosis instrument is manufactured with this mechanism.

Objective To investigate the correlation between histone deacetylase 1(HDAC1) and vascular endothelial growth factor(VEGF) in the patients with lung adenocarcinoma.Methods Eighty cases of lung adenocarcinoma in our hospital from August 2014 to April 2016 served as the research subjects,and contemporaneous 80 individuals undergoing healthy physical examination were taken as the control group.The fasting venous blood sample was collected in all subjects.Then serum HDAC1 and VEGF levels were detected by ELISA.The differences of serum HDAC1 and VEGF expression levels were compared between the two groups.The HDAC1 and VEGF expression levels in the patients with different characteristics of lung adenocarcinoma and the relation between serum HDAC1 and VEGF concentrations were analyzed.Furthermore the possible influence factors of HDAC1 protein expression level in the patients with lung adenocarcinoma were analyzed.Results The HDAC1 levels in the control group and observation group were(329.56 ± 23.83) ng/L and(568.20 ± 35.40) ng/L,the difference was statistically significant(t=23.576,P=0.000).The VEGF levels in the control group and observation group were(40.26±9.82)ng/L and(296.56±19.80)ng/L respec tively,the difference was statistically significant(t=31.154,P=0.000).The HDAC1 protein level had statistical difference among different genders,ages,clinical stages and smoking history,the HDAC1 protein level in male,age ＞60 years old,clinical stage Ⅲ,V and patients with smoking history were higher(P＜0.05).The Pearson correlation analysis results showed that serum HDAC1 in the patients with lung adenocarcinoma was positively correlated with VEGF protein concentration(r=0.526,P =0.000).The Logistic regression analysis showed that influence factor of HDAC1 protein expression level in the patients with lung adenocarcinoma was clinical stage.Conclusion The high expression of HDAC1 protein in lung adenocarcinoma patients may also simultaneously regulate the VEGF expression,thus promotes the development of lung adenocarcinoma.

Objective:To evaluate the effect of down-regulating lncRNA LINC00263 targeting miR-4458 on the proliferation, migration, invasion and radiosensitivity of breast cancer SK-BR-3 cells.Methods:The expression differences of LINC00263 in breast cancer tissues, adjacent tissues, normal breast epithelial cells and breast cancer cells were determined by qRT-PCR. Transfection of LINC00263 shRNA in breast cancer SK-BR-3 cells down-regulated the expression of LINC00263, and the cloning experiment was used to detect the radiosensitivity. Breast cancer SK-BR-3 cells were treated with 6 Gy irradiation. CCK-8 assay was employed to detect cell proliferation. Flow cytometry was adopted to detect cell apoptosis. Transwell chamber test was performed to detect cell migration and invasion. Western blot was used to detect the expression levels of C-Caspase-3 and C-Caspase-9, MMP-2 and MMP-9 proteins. Bioinformatics software predicted that LINC00263 and miR-4458 had complementary binding sites, and the luciferase reporter system was utilized determine the targeting relationship between LINC00263 and miR-4458. LINC00263 shRNA and miR-4458 inhibitor were co-transfected into breast cancer SK-BR-3 cells, and 6 Gy irradiation was given to detect the changes in cell proliferation, apoptosis, invasion and migration.Results:The expression level of LINC00263 in breast cancer tissues was higher than that in adjacent tissues. The expression level of LINC00263 in breast cancer cells was higher compared with that in normal breast epithelial cells. The radiosensitivity of breast cancer SK-BR-3 cells was increased after transfection of LINC00263 shRNA. Transfection of LINC00263 shRNA and radiation exerted a synergistic effect, jointly inhibited breast cancer cell proliferation, migration and invasion, promoted cell apoptosis, up-regulated the expression levels of C-Caspase-3 and C-Caspase-9 proteins in cells, and down-regulated those of MMP-2 and MMP-9 proteins. Down-regulation of LINC00263 targetedly up-regulated miR-4458 expression. miR-4458 inhibitor reversed the inhibitory effect of LINC00263 shRNA combined with radiation on the proliferation, migration, invasion and apoptosis promotion of breast cancer SK-BR-3 cells.Conclusion:Down-regulating lncRNA LINC00263 targeting miR-4458 inhibits the proliferation, migration and invasion of breast cancer SK-BR-3 cells, and improves cell radiosensitivity.

Objective: To investigate the expression of lncRNA01296 in esophageal cancer (EC) tissues and its effect on the proliferation and migration of EC TE-2 cells. Methods:Atotal of 36 pairs of esophageal cancer tissues and corresponding para-cancerous tissues were collected from EC patients admitted to the Department of Thoracic Surgery,Affiliated Hospital of Chengde Medical College from January 2017 to September 2018. The human normal esophageal epithelial (HEEC) cells and human esophageal cancer cell lines ECA109, TE-1 and TE-2 were cultured. qPCR was used to detect the mRNAexpressions of lincRNA01296, SNRPA(small nuclear ribonucleoproteinA) and NGF (nerve growth factor) in EC tissues and cells. Recombinant lentiviral interference vectoror control vector were used to transfect EC cell lines, as sh-lncRNA01296#1,#2 and Mock groups. WB was used to detect the protein expressions of SNRPAand NGF in transfected cells. MTS assay was used to detect cell proliferation, and Transwell assays were used to detect cell invasion and migration of TE-2 cells after transfection. Results: The mRNAexpressions of lncRNA01296, SNRPAand NGF were significantly increased in esophageal cancer tissues and cell lines (all P<0.01), and these expressions in poorly differentiated TE-2 cells were higher than those in highly differentiated ECA109 and TE-1 cells (all P<0.05). The mRNAexpressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01), while the mRNAexpression of SNRPAshowed no statistical difference among three groups (P>0.05). The protein expressions of lncRNA01296 and NGF in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly lower than those in Mock group (all P<0.01). The relative proliferation ability of cells in sh-lncRNA01296#1 and shlncRNA01296#2 groups was significantly lower than that of Mock group at 48 and 72 h after transfection (P<0.05 or P<0.01). The number of invasive cells was (72.0±6.3), (36.6±4.3) and (33.9±3.7) in Mock, sh-lncRNA01296#1 and sh-lncRNA01296#2 groups, respectively; and the number of migrated cells was (85.2±9.9), (47.5±8.1) and (43.8±6.5), respectively, indicating that the numbers of invasive and migrated cells in sh-lncRNA01296#1 and sh-lncRNA01296#2 groups were significantly less than those in Mock group(all P<0.01). Conclusion: lncRNA01296 can up-regulate SNRPAexpression to promote NGF-mediated proliferation and metastasis of EC cells, which may provide new target for the diagnosis and treatment of esophagealcancer.