Objective To evaluate the effect of the gastric signet ring cell cancer(SIG)on the T,N,M stages. Methods Three hundred and fifty-one patients undergoing D2 or greater gastrectomy for gastric cancer were ana lyzed retrospectively.The T,N,M stages of 59 patients with SIG and 161 patients with tubular adenocarcmonla (TUB)were compared using univariate and multivariate analysis.Results The chi-square test showed that there were not significant differences in T,N,M stages between TUB and SIG.Multivariate Logistic regression analysis indicated that SIG Was not a independent factor influencing the T,N.M stage.Conclusion Gastric cancer with SIG has not higher T,N,M stages than that with TUB.

Objective To investigate NIMA-related kinase 2 (NEK2) expression in colorectal cancer (CRC) tissues and its effect on the proliferation, migration and invasion of HCT116 cells. Methods Synthesized siRNA targeting NEK2 was transfected into HCT116 cells by lipofectamine method. CCK8 assay, FACS, wound healing assay and Transwell assay were used to detect the effects of NEK2 knockdown on cell proliferation, cell cycle distribution, migration and invasion. Western blot was carried out to detect the expression of E-cadherin, N-cadherin, CDK4 and cyclin D1. Results The expression of NEK2 in CRC tissues was significantly higher than that in adjacent normal tissues (65.0% vs. 35.0%, χ²=14.593, P < 0.01), and its level was closely related to TNM stage, lymph node metastasis and distant metastasis (all P < 0.05). NEK2 protein and mRNA levels in CRC cell lines were also significantly higher than those in normal colorectal mucosal cells (P < 0.01). After NEK2 was knocked down by siRNA, HCT116 cells were arrested in G₀/G₁ cycle, while cell proliferation, invasion and migration were significantly reduced (P < 0.01). NEK2 interference in HCT-116 cells led to the upregulation of E-cadherin and downregulation of N-cadherin, CDK4 and cyclin D1 at protein levels. Conclusion The high NEK2 expression is correlated with clinicopathological characteristics of CRC patients. NEK2 knockdown by siRNA could effectively inhibit the proliferation, invasion and migration abilities of colorectal cancer cells, suggesting that NEK2 plays an important role in the occurrence and development of colorectal cancer and it can be used as a potential treatment target.

Objective:To investigate the mechanism of Coptidis rhizoma in the treatment of gastritis based on network pharmacology. Methods:The main components and targets of Coptidis rhizoma were screened by TCMSP and TCMID database. GeneCards were used to select the target genes related to gastritis from the human gene database, and the target genes related to gastritis were screened by Genemap in the OMIM database. We used R language VennDiagram package to crosse the gene targets of drugs and diseases, and screen the target of the main components of Coptidis rhizoma in the treatment of gastritis, and to use Cytoscape software to map the gene regulatory network of galangal in the treatment of gastritis, and to use the String database to construct the gene-protein of Coptidis rhizoma. The interaction visualization network map for protein- protein interaction (PPI) were screened out the core genes, and the Bioconductor in the R language was used to analyze the GO and KEGG pathways for the selected gene targets. Results:Fourteen main active compounds of Coptidis rhizoma were screened, and 71 gene targets may be involved in the treatment of gastritis. The results of GO and KEGG pathway analysis indicated that berberine mainly involves cytokine receptor binding, regulation of cytokine activity, and biological processes such as binding to heme, by regulating AGE-RAGE, IL-17, TNF, NF-kappa B and HIF-1. The signaling pathway acts to treat gastritis. Conclusions:This study constructed the role of berberine in the treatment of gastritis with multi-active component, multi-gene, multi-target pathway through network pharmacology. It comprehensively predicted the gene target and signaling pathway of Coptidis rhizoma in the treatment of gastritis, in order to further study the treatment of berberine. The mechanism of action of gastritis provides a reference basis.

Objective: To explore the expression of IQGAP1 (Ras GTPase-activating-like protein containing IQ domain) in esophageal squamous cell carcinoma (ESCC) tissues and cell lines and its effect on the proliferation and invasion of TE-2 cell. Methods: Totally 125 pairs of cancer tissues and para-cancerous tissues from ESCC patients, who underwent surgical resection inAffiliated Tumor Hospital of Zhengzhou University from January 2015 to December 2016, were included in this study; in addition, ESCC cell lines (TE-2, TE3, ECA109) and normal esophageal epithelial cell line Het-1A were also collected. The expression of IQGAP1 was detected by immunohistochemical staining and its relationship with cliniopathological features was also analyzed. IQGAP1 mRNA and protein expressions in ESCC cell lines were detected by Real-time quantitative PCR (qPCR) and Western blotting, respectively. TE-2 cells were transfected with si-IQGAP1 (positive transfection group) and si-CTRL (negative control group) plasmids, and the effects of IQGAP1 silencing on the proliferation and invasion of TE-2 cells were detected by MTT and Transwell assay. The expressions of E-cadherin and Ncadherin were detected by Western blotting. Results: The positive expression rate of IQGAP1 in ESCC tissues was significantly higher than that in para-cancerous tissues (P<0.05), which was closely related to tumor stage and histologic grade (all P<0.05). The mRNAand protein expressions of IQGAP1 in TE-2, TE-3 and ECA109 cells were significantly higher than those in Het-1Acells (all P<0.05).After IQGAP1 was silenced, compared with the negative control group and the blank group, the expression of IQGAP1 mRNAand protein in the positive transfection group significantly decreased (all P<0.05); the proliferation and invasiveness of TE-2 cells significantly decreased (all P<0.05); E-cardherin was up-regulated while N-cardherin was down-regulated (all P<0.05) in the positive interference group. Conclusion: IQGAP1 is highly expressed in ESCC tissues, and si-IQGAP1 can inhibit the proliferation and invasion of TE-2 cells, which plays an important role in the occurrence and development of ESCC.