Silencing of MAP4K4 by short hairpin RNA suppresses proliferation, induces G1 cell cycle arrest and induces apoptosis in gastric cancer cells.

Gastric cancer (GC) is the second most common cause of cancer‑associated mortality worldwide. Previous studies suggest that mitogen‑activated protein kinase kinase kinase kinase isoform 4 (MAP4K4) is involved in cancer cell growth, apoptosis and migration. In the present study, bioinformatics analysis and reverse transcription‑quantitative polymerase chain reaction were performed to determine if MAP4K4 was overexpressed in GC.

Effect of RTKN on progression and metastasis of colon cancer in vitro.

Like many epithelial-derived cancers, colon cancer results from a multistep tumorigenic process. However, the detailed mechanisms involved in colon cancer formations are poorly characterized. In the present study, we investigated the role of RTKN in colon cancer and explored underlying mechanisms.

Ponicidin induces apoptosis via JAK2 and STAT3 signaling pathways in gastric carcinoma.

Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8).

[Changes of tight junction claudin-1,-3,-4 protein expression in the intestinal mucosa in patients with irritable bowel syndrome].

Objective: To investigate the changes of intestinal mucosal tight junction proteins claudin-1, -3, -4 in patients with irritable bowel syndrome (IBS), and elucidate its possible role in the bowel evacuation habit changes and formation in these patients.

Methods: Western blotting was employed to determine tight junction protein claudin-1,-3,-4 levels in the intestinal mucosa of patients in the control group, diarrhea-predominant IBS (D-IBS) group and constipation-predominant IBS (C-IBS) group.

Results: Compared with the control group, D-IBS patients showed significantly decreased claudin-1 protein levels in both the small intestinal and colonic mucosae (P<0.

[Changes in tight junction of intestinal mucosa in patients with irritable bowel syndrome: a study with tracing electron microscope].

Objective: To investigate the presence of tight junction (TJ) changes of the intestinal mucosa, and elucidate the possible mechanism for changes in bowel evacuation in patients with irritable bowel syndrome (IBS).

Methods: In 10 normal control subjects, 10 patients with constipation predominant IBS (C-IBS) and 10 with diarrhea predominant IBS (D-IBS), biopsies were taken from the terminal ileum and ascending colon. Lanthanum nitrate tracing electron microscope and cytochemical technique were employed to observe TJ changes in the intestinal mucosa.

Effect of change in an inhibitory neurotransmitter of the myenteric plexus on the pathogenetic mechanism of irritable bowel syndrome subgroups in rat models.

Objective: In order to investigate the effect of change in an inhibitory neurotransmitter of the myenteric plexus on irritable bowel syndrome (IBS) subgroups, the amounts of nitric oxide (NO) in constipation-predominant (C-IBS) and diarrhea-predominant (D-IBS) IBS models in rats were studied.

Methods: The D-IBS model was created in rats by intracolonic instillation of acetic acid and by restraint stress. The D-IBS control group underwent intracolonic instillation with saline instead.