Exploring the role of LINC-ROR in epithelial-mesenchymal transition and its correlation with CD44 and TWIST1 in gastric cancer progression

Abstract

Background

Gastric cancer (GC) is a leading cause of cancer-related mortality, characterized by its intricate etiology and aggressive nature. The interplay between coding and non-coding RNAs facilitates the identification of protein-protein interaction networks, which are crucial for understanding the prognosis, incidence, diagnosis, and treatment of cancer. This study aims to investigate the clinical significance of co-expression of lncRNA regulator of reprogramming (LINC-ROR), TWIST1, and CD44 in GC, offering valuable insights into the disease's pathogenesis and potential therapeutic targets.

Materials and methods

Quantitative real-time PCR was employed to compare the expression profiles of LINC-ROR, TWIST1, and CD44 in 86 paired tumor and adjacent normal tissue samples obtained from GC patients who underwent curative surgery. The expression levels of LINC-ROR, TWIST1, and CD44 were canalyzed to evaluate their co-expression patterns and determine their clinical significance in GC.

Results

Our findings demonstrated that the concomitant expression of LINC-ROR and CD44 was significantly correlated with lymph node invasion and early tumor stages (I/II) (P < 0.05). Moreover, the co-expression of LINC-ROR and CD44 with TWIST1 correlated with tumor grade II and stages I/II of tumor progression (P < 0.05). Notably, LINC-ROR was underexpressed in 54.7 % of tumors, while TWIST1 and CD44 were overexpressed in 53.5 % and 50 % of cases, respectively (P < 0.0001). The dysregulation of these markers was significantly linked to severalclinical factors, including sex, tumor stage, H. pylori, grade, type, and location of tumor (P < 0.05).

Conclusion

Our findings emphasize the regulatory role of LINC-ROR in EMT processes and GC progression, highlighting its potential as a biomarker for prognosis and therapeutic targets in GC management. This study  enhances our understanding of the icomplex  molecular interactions that underlie GC pathogenesis.