Association of Poor Sleep Quality With Adverse Outcomes in Patients With Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis.

Objectives: Inflammatory bowel disease (IBD) is a group of chronic diseases with adverse events such as disease flare, progression, drug escalation, hospitalization, and surgery. Meanwhile, patients with IBD often have sleep disorders. We performed this systematic review and meta-analysis aiming to investigate the relationship between sleep quality of patients with IBD and their prognosis.

Screening of potential diagnostic markers and therapeutic targets against colorectal cancer.

Objective: To identify genes with aberrant promoter methylation for developing novel diagnostic markers and therapeutic targets against primary colorectal cancer (CRC).

Methods: Two paired CRC and adjacent normal tissues were collected from two CRC patients. A Resi: MBD2b protein-sepharose-4B column was used to enrich the methylated DNA fragments.

Synbindin in extracellular signal-regulated protein kinase spatial regulation and gastric cancer aggressiveness.

Background: The molecular mechanisms that control the aggressiveness of gastric cancer (GC) remain poorly defined. Here we show that synbindin contributes to the aggressiveness of GC by activating extracellular signal-regulated protein kinase (ERK) signaling on the Golgi apparatus.

Methods: Expression of synbindin was examined in normal gastric mucosa (n = 44), intestinal metaplastic gastric mucosa (n = 66), and GC tissues (n=52), and the biological effects of synbindin on tumor growth and ERK signaling were detected in cultured cells, nude mice, and human tissue samples.

The role of ERK2 in colorectal carcinogenesis is partly regulated by TRAPPC4.

The extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK) pathway is an important cell proliferation pathway. We previously reported that the transport protein particle complex 4 (TRAPPC4), ERK2 interaction may activate ERK1/2, modulate pERK2 nuclear localization and regulate proliferation and apoptosis in colorectal cancer (CRC) cells. The present study further investigated the function of the TRAPPC4-ERK2 interaction in CRC in vitro and in vivo.

TRAPPC4-ERK2 interaction activates ERK1/2, modulates its nuclear localization and regulates proliferation and apoptosis of colorectal cancer cells.

The trafficking protein particle complex 4 (TRAPPC4) is implicated in vesicle-mediated transport, but its association with disease has rarely been reported. We explored its potential interaction with ERK2, part of the ERK1/2 complex in the Extracellular Signal-regulated Kinase/ Mitogen-activated Protein Kinase (ERK-MAPK) pathway, by a yeast two-hybrid screen and confirmed by co-immunoprecipitation (Co-IP) and glutathione S-transferase (GST) pull-down. Further investigation found that when TRAPPC4 was depleted, activated ERK1/2 specifically decreased in the nucleus, which was accompanied with cell growth suppression and apoptosis in colorectal cancer (CRC) cells.

MicroRNA 345, a methylation-sensitive microRNA is involved in cell proliferation and invasion in human colorectal cancer.

Aberrant methylation has been shown to trigger the inactivation of tumor suppressor genes during tumorigenesis. MicroRNAs (miRNAs) have been found deregulated in human colorectal cancer (CRC), and some of them may function as tumor suppressor genes. Here, we investigated CpG island promoter hypermethylation as a potential mechanism underlying miRNA disruption and identifed methylation-sensitive miRNAs that might repress CRC development.

Combined inhibition of Dnmt and mTOR signaling inhibits formation and growth of colorectal cancer.

Background And Aims: Although the anticancer effects of rapamycin (RPM) and 5-aza-deoxycytidine (AZA) have been studied extensively, the combined effect of these two drugs on colorectal cancer (CRC) is still unknown. This study addresses the effect of AZA and RPM combination therapy on CRC and its influence on the mammalian target of rapamycin (mTOR) and its signal transduction pathway.

Subjects And Methods: Human CRC cell line HCT116 was treated with AZA alone, RPM alone, or concurrently with a combination of both drugs.

Combined inhibition of MEK and mTOR signaling inhibits initiation and progression of colorectal cancer.

The role of the mTOR signal pathway in colorectal cancer (CRC) pathogenesis remains unclear, and the combination effect of PD98059 (an inhibitor for MEK) and rapamycin (an inhibitor for mTOR) on CRC is still unknown. Here, we found that combination treatment with PD98059 and rapamycin suppressed the proliferation of CRC cells, induced apoptosis, arrested cell cycle, and reduced the incidence and volume of CRC in mice, as well as inhibited phosphorylation of mTOR and the MEK signal pathway components, of which the effects were more significant than single-drug treatments. These findings indicate that PD98059 combined with rapamycin appears to be a promising strategy for inhibiting the initiation, and progression of CRC, which may provide a novel strategy for CRC prevention.

Folic acid and sodium butyrate prevent tumorigenesis in a mouse model of colorectal cancer.

Colorectal cancer is a leading cause of morbidity and mortality worldwide, and its incidence has been increasing in recent years. The role of epigenetic modifications, including DNA methylation and histone modifications, has only recently been investigated. In this study, the effects of epigenetic agents such as folic acid (FA) and sodium butyrate (NaBu) on the development of colorectal cancer induced by 1,2-dimethylhydrazine (DMH) using ICR mice was examined.

[Synergistic effect of rapamycin (RPM) and PD98059 on cell cycle and mTOR signal transduction in human colorectal cancer cells].

Objective: To investigate the synergistic effect of rapamycin (RPM) and PD98059 on human colorectal cancer cells and its potential mechanisms.

Methods: Three human colorectal cancer cell lines SW480, HCT116 and HT29 were treated with RPM 10 nmol/L, PD98059 (10 micromol/L, 20 micromol/L, 40 micromol/L, 50 micromol/L), or RPM plus PD98059, respectively, and the sensitivity was analyzed by MTT assay. The cell cycle progression was evaluated by flow cytometry.

The role of postoperative adjuvant chemotherapy following curative resection for gastric cancer: a meta-analysis.

To evaluate the effect of adjuvant chemotherapy on survival rates after curative resection of gastric cancer, MEDLINE (1969-2006), EMBASE (1974-2006), bibliographies, and review articles were searched for relevant articles. The meta-analysis was finally based on 15 trials that included 3212 patients. RR for death in the treated group was 0.