Furthermore, ectopic expression of Wnt1 or suppression of GSK-3β abolished the si-LINC01225-mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC.
Evidence indicates that wingless-type MMTV integration site family, member 1 (WNT1)-inducible signaling pathway protein 2 (WISP2) may play an important role in the development of gastric cancer (GC) by regulating the WNT/β-catenin signaling pathway.
In addition, our data demonstrated that hTERT activated Wnt/β-catenin signaling to promote c-Myc expression which could in turn activate hTERT transcription and expression, suggesting a positive feedback regulation in GC progression.
Increased Hspa5 and Chop expression were found in dysplasia of C57Bl/6 mice with chronic H. felis infection but was absent in spontaneous gastric dysplasia in K19-Wnt1/C2mE mice with concomitant loss of Mist1 expression, similar to that observed in H. pylori-associated human GC.