MAPK pathways are involved in the inhibitory effect of berberine hydrochloride on gastric cancer MGC 803 cell proliferation and IL-8 secretion invitro and invivo.

Abstract

Gastric cancer is the second leading cause of cancer-associated mortality worldwide. This investigation aimed to identify whether the mitogen‑activated protein kinase (MAPK) signaling pathways are involved in the inhibitory effect of berberine hydrochloride (BER) on MGC803cells invitro and invivo. BER time‑ and dose‑dependently inhibited proliferation of MGC803cells. It also suppressed tumorigenesis in nude mice xenografted with MGC803cells. Additionally, BER reduced interleukin‑8 (IL‑8) secretion invitro and invivo. Further investigation demonstrated that inactivation of p38 MAPK, extracellular-signal regulated kinase1/2 and c‑Jun N‑terminal kinase by BER contributed to the decreased proliferation and tumorigenesis, and the change in IL‑8 expression levels. However, there was no significant synergistic inhibitory effect of combined BER and evodiamine (EVO) treatment on tumorigenesis, and BER reduced the upregulation of IL‑8 induced by EVO invivo. The results of the current study suggested that BER may be an effective and safe drug candidate for treating gastric cancer via modulation of the MAPK signaling pathways.