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J Cell Physiol. 2018 Jun;233(6):4634-4642. doi: 10.1002/jcp.26190. Epub 2018 Jan 15.

Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling.

Author information

1
Department of Gastrointestinal Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, P.R. China.

Abstract

In this study, we aimed to investigate the effects of curcumin on cell activities of gastric cancer (GC), and the connection between curcumin and P53, as well as, PI3K signaling. This study was conducted with two cell lines SGC-7901 and BGC-823, both were exposed to curcumin at the concentrations of 0, 10, 20, and 40 μm. MTT assay, flow cytometry (FCM) assay, transmission electron microscopy (TEM) were used to study the underlying mechanisms of curcumin in respective of proliferation, apoptosis, and autophagy. Western blot assay was also employed to detect impacts of curcumin on tophosphatidylinositol-3 kinase (PI3K) and P53 signaling pathways-related proteins. MTT assay displayed that curcumin inhibited GC cell proliferation. FCM results indicated that curcumin induced the apoptosis of GC cells. TEM revealed that curcumin induced autophagy in GC cells. Western blot results showed that curcumin activated P53 signaling pathway and inhibited PI3K signaling pathway. Curcumin may inhibit proliferation and induce the autophagy and apoptosis in GC cells. Additionally, curcumin activated the P53 signaling pathway by up-regulating P53 and P21, which also inhibited PI3K pathway through down-regulating PI3K, p-Akt, and p-mTOR.

KEYWORDS:

P53; PI3K; curcumin; gastric cancer

PMID:
28926094
DOI:
10.1002/jcp.26190
[Indexed for MEDLINE]

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