upregulation is associated with chromatin remodeling in gastric cancer and induction of tumorigenicity in a xenograft mouse model.

Pathological changes in the epigenetic landscape of chromatin are hallmarks of cancer. Our previous study showed that global methylation of promoters may increase or decrease during the transition from gastric mucosa to intestinal metaplasia (IM) to gastric cancer (GC). Here, CpG hypomethylation of the serine/threonine kinase promoter in IM and GC was detected in a reduced representation bisulfite sequencing database. hypomethylation, which resulted in its upregulation in 120 cases of primary GC, was confirmed. Using public genome‑wide histone modification data, upregulation of promoter activity was detected in primary GC but not in normal mucosae, suggesting that may be repressed in gastric mucosa but activated in GC as a consequence of hypomethylation‑associated chromatin remodeling. knockdown suppressed the proliferation, colony formation and migration activities of GC cells , whereas stable overexpression of STK31 promoted the proliferation, colony formation, and migration activities of GC cells and tumorigenesis in nude mice. Patients with GC in which was upregulated exhibited significantly shorter survival times in a combined cohort. Thus, activation of by chromatin remodeling may be associated with gastric carcinogenesis and also may help predict GC prognosis.