Objective: To investigate the expression of Runt-related transcription factor gene 3(RUNX3) in gastric cancer and its impact on the outcome of gastric cancer patients.

Methods: By using immunohistochemistry staining and western blot assay, the expression of RUNX3 protein in 66 cases of gastric cancer with various clinicopathologic characteristics were detected, and the effects of RUNX3 protein expression on the outcome of patients undergone surgical resection were evaluated.

Results: (1) The expression rate of RUNX3 protein in gastric cancer lesions was 60.6% (40/66), and RUNX3 protein was mainly expressed in the cytoplasm of cancer cells. RUNX3 protein expression in tumor tissues was significantly higher than that in non-tumor tissues. (2) RUNX3 protein expression was correlated with tumor differentiation (P=0.025) and Lauren's classification (P=0.034), but had no relationship with the TNM stage (P=0.085). (3) In sharp contrast, the median survival time of patients who had tumors with negative and positive RUNX3 protein expression were 2478 and 2187 days respectively (P=0.016).

Conclusions: RUNX3 protein influences the differentiation of gastric cancer. The role of RUNX3 protein as a tumor-suppressor in tumorigenesis and differentiation of gastric carcinoma need to be further evaluated.

Download full-text PDF

Source

Publication Analysis

Top Keywords

runx3 protein
36
gastric cancer
20
protein expression
16
runx3
9
protein
9
runt-related transcription
8
transcription factor
8
factor gene
8
expression
8
differentiation gastric
8

Similar Publications

The scaffold protein AMBRA1, which participates in the autophagy pathway, also promotes CD4 T cell differentiation to Tregs independent of autophagy through its interactor PP2A. Here we have investigated the role of AMBRA1 in CD8 T cell differentiation to cytotoxic T cells (CTL). AMBRA1 depletion in CD8 T cells was associated with impaired expression of the transcription factors RUNX3 and T-BET that drive CTL differentiation and resulted in impaired acquisition of cytotoxic potential.

View Article and Find Full Text PDF

Background: To avoid exaggerated inflammation, innate immune cells adapt to become hypo-responsive or "tolerance" in response to successive exposure to stimuli, which is a part of innate immune memory. Polycomb repressive complex 2 (PRC2) mediates the transcriptional repression by catalyzing histone H3 lysine 27 trimethylation (H3K27me3) but little is known about its role in lipopolysaccharide (LPS)-induced tolerance in macrophages.

Result: We examined the unexplored roles of EED, a component of the PRC2, in LPS tolerant macrophages.

View Article and Find Full Text PDF

Purpose: Our research aimed to evaluate whether proto-oncogene serine/threonine-protein kinase Pim-1 (Pim1) inactivation could attenuate asthma by promoting runt-related transcription factor 3 (Runx3) expression and explore the underlying molecular mechanism.

Method: Phorbol 12-myristate 13-acetate (PMA, 50 nM) was used to induce inflammation in BEAS-2B human airway epithelial cells. ELISA and immunofluorescence double staining confirmed inflammation modelling and differential expression of Pim1 and Runx3.

View Article and Find Full Text PDF
Article Synopsis
  • The study focuses on the tumor immune microenvironment, particularly the roles of regulatory T cells (Tregs) and cytotoxic T cells (CD8+), as factors influencing prognosis in aggressive gastroesophageal adenocarcinomas (GEAs).
  • It found that a high FOXP3+/CD8+ cell ratio at the invasive margin of tumors correlates with worse survival outcomes, especially in RUNX3-methylated diffuse variants compared to intestinal types.
  • The research suggests that increased FOXP3+/CD8+ ratios may facilitate immune evasion in tumors, potentially linked to the signaling molecule CCL28 and its relationship with RUNX3 methylation status.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!