Thus, these findings elucidate a novel mechanism by which PPARδ promotes gastric tumorigenesis through interaction with YAP1 and highlights the PPARδ/YAP1/SOX9 axis as a novel therapeutic target in human GC.
Current evidence highlights the key function of SOX9 in GC and postulates it as a prognostic factor, novel biomarker for patient stratification and a promising target. gCSCs are critical targets for GC eradication and SOX9 is a regulator of gCSCs; hence, the inhibition of SOX9 is a potential therapeutic strategy for GC, particularly for the MSS/TP53+ subgroup of patients in whom SOX9 expression correlates with poor outcome.
The current study revealed that SOX9 may be involved in the pathogenesis of GC, and further elucidation of the pathways involved may support the development of novel therapeutic options for the treatment of GC.
SOX9 expression and its methylation status in six GC cell lines, their Epstein-Barr virus (EBV)-infected cell lines, and two EBV-associated GC cell lines was also examined.
As to molecular events in individual mucin phenotypes of gastric cancer, the CDX2-Reg IV-SOX9 pathway is associated with the intestinal mucin phenotype, while OLFM4 and CLDN18 are novel markers for the gastric phenotype. microRNAs play an important role in epigenetic deregulation in gastric cancer.