Abstract 166P
Background
The development of gastric cancer (GC) is mainly dependent on chronic inflammation and cellular stress, both of which are greatly exacerbated by Helicobacter pylori infection. Considering the role of GRP and CHOP in the apoptosis resistance and survival of CSCs, their correct function in the cell is vital. Our aim in this study was to investigate the probable correlation between stemness markers in response to cellular stress conditions, with particular attention to their potential association with GC development. We evaluated the potential association between the expression of CHOP, GRP94, CD44, and SALL4 with various clinical parameters to find a potential strategy for identifying cancer cells and monitoring the effectiveness of treatment in patients.
Methods
The study analyzed the mRNA expression profiling of CHOP, GRP94, CD44, and SALL4 in GC tissues and adjacent non-cancerous tissues using quantitative real-time PCR. Clinicopathologic and RNA-Seq gene expression data of gastric cancer patients were extracted from Gene Expression Omnibus database.
Results
Overexpression of CHOP, GRP94, CD44, and SALL4 were displayed in 22% (32/86), 27% (39/86), 30% (43/86), and 35% (49/86) GC samples, respectively. Dysregulation of GRP94 and CHOP was significantly related to metastasis to the lymphatic nodes and H. pylori infection (P < 0.05). While there was a significant correlation between CD44 and SALL4 expression and H. pylori infection (P < 0.05). Moreover, the expression pattern of CD44 was significantly associated with the type of tumor (P < 0.05). The results indicated a significant correlation between concomitant expression of CHOP, GRP94, CD44, and SALL4 with each other in a variety of clinicopathological traits in GC tissue samples (P < 0.05).
Conclusions
Our findings confirmed that dysregulation of CHOP, GRP94, CD44, and SALL4 was related to pathogenesis, invasive phenotype, metastasis, and poor prognosis in GC patients. Our results demonstrated the interplay between the CSC-like phenotype, the induction of inflammation, and the ER stress-mediated apoptosis pathway in GC development, proposing a potential target axis for the development of therapeutic strategies and mechanisms involved in GC.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
Mashhad University of Medical Sciences.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.