Objective:To study the clinical value of peripheral blood Runx3 gene CpG island's methylation in the evaluation of colon cancer's disease condition and prognosis.Methods:Methy1ation specific PCR was used to detect the Runx3 gene CpG island's methylation by Peripheral blood in colon cancer patient (observation group) and healthy people (control group).The Runx3 gene CpG island's methylation rates in different clinicopathological factors were compared.The 3 year survival rate and total survival time between patient with Runx3 gene CpG island's methylation and unmethylation were Compared.Result:The Runx3 gene CpG island's methylation rate in observation group was significantly higher than in control group (P＜0.05).The Runx3 gene CpG island's methylation rates in degree of differentiation,maximum tumor diameter,lymph node metastasis,distant metastasis,TNM staging and surgical resection were significant different (P＜0.05).The 3 year survival rate and total survival time in patient with Runx3 gene CpG island's methylation were significantly higher than in patient with Runx3 gene CpG island's unmethylation.Conclusion:Runx3 gene CpG island is hypermethylated in colon cancer's peripheral blood,which has value in the evaluation of colon cancer's disease condition and prognosis.

Objective To investigate the inhibitory effect of 5-fluorouracil (5-FU) on hepatocellular carcinoma (HCC) cell growth and to elucidate its potential molecular mechanism.Methods Real-time PCR analysis was conducted to determine the expression of miR-373 in HCC tissue specimens and HCC cell lines.The expression of miR-373 was also evaluated in HepG2 cells after 5-FU treatment.Western blot analysis was performed to detect the protein levels of PPP6C,a verified target of miR-373,with transfection of miR-373 mimics or 5-FU treatment.A rescue assay was conducted to investigate the cell growth in HepG2 cells by using CCK-8.Results miR-373 expression was up-regulated in both HCC tissues and cell lines.miR-373 expression depicted about 2.94-fold augment in HepG2 cells as compared to normal liver cells control (P ＜0.01).5-FU treatment led to a significant decrease of miR-373 levels (approximately 50％,P ＜0.01,48 h) and resulted in a marked increase of PPP6C protein (approximately 2.1-fold,48 h) in HepG2 cells.The overexpression of miR-373 could prevent the impact of 5-FU treatment on cell growth in HepG2 cells and CCK-8 assay showed that HepG2 cell growth was rescued approximately 81％ and 84％ at 24 h (P ＜ 0.05) and 48 h (P ＜ 0.01),respectively.Conclusion 5-FU can repress endogenous miR-373 level,which activates the expression of downstream targeted gene PPP6C,thereby exerting an inhibitory effect on HepG2 cells.

This article reviews the research advances in the characteristics and application progress of various new models for preclinical cancer research on pancreatic cancer， analyzes and discusses the history， current research status， and advantages and disadvantages of new models of pancreatic cancer， including patient-derived tissue xenograft， conditional reprogramming， and patient derived organoids， and it also reviews the studies that have achieved clinical transformation from preclinical models and proposes possible research prospects in the future.