Jumonji AT-rich interactive domain 1B promotes the growth of pancreatic tumors via the phosphatase and tensin homolog/protein kinase B signaling pathway.

Abstract

Jumonji AT-rich interactive domain 1B (JARID1B) has been revealed to remove methyl residues from methylated lysine 4 on histone H3 (H3K4) and has also been reported to be associated with the progression of numerous types of tumor. However, its roles and mechanisms in pancreatic cancer (PC) remain unknown. The present study demonstrated that JARID1B is elevated in PC and is associated with the growth of pancreatic tumors. Overexpression of JARID1B significantly promoted the proliferation in vitro and tumor formation in vivo of PC cells. Furthermore, silencing the expression of JARID1B in other PC cells revealed opposite effects. Further research revealed that JARID1B exerted its function through modulation of H3K4me3 at the phosphatase and tensin homolog (PTEN) gene promoter which was associated with inactive PTEN transcription. To the best of our knowledge, the present study was the first to demonstrate that JARID1B promotes the growth of PC and that targeting JARID1B may be a useful strategy to suppress the progression of PC.