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Clin Transl Oncol. 2016 May;18(5):521-6. doi: 10.1007/s12094-015-1399-3. Epub 2015 Oct 21.

The effect of EGB on proliferation of gastric carcinoma SGC7901 cells.

Author information

1
Department of General Surgery, The Affiliated 2ed Hospital of Nantong University, 6 Baby Lane North Road, Nantong, 226001, Jiangsu Province, China.
2
Department of Neurosurgery, Zhejiang Cancer Hospital, 38 Guangji Road, Hangzhou, 310022, Zhejiang Province, China.
3
Department of General Surgery, The Affiliated 2ed Hospital of Nantong University, 6 Baby Lane North Road, Nantong, 226001, Jiangsu Province, China. SunYongqiangdocdoc@163.com.

Abstract

OBJECTIVE:

To investigate the effect of Ginkgo biloba extract (EGB) on the proliferation and cell cycles of gastric carcinoma SGC7901 cells, and make a preliminary exploration on possible molecular mechanisms associated with its inhibitory effect.

METHODS:

Human gastric carcinoma SGC7901 cells were cultured in vitro, and treated with various concentrations (100, 200, 300, 400 mg/L) of EGB for different incubation periods (24, 48 and 72 h). CCK-8 assay was used to detect cell proliferation and flow cytometry was performed to analyze the effect of EGB on cell cycles. In addition, mRNA and protein level of two cell cycle regulators cyclin D1 and c-myc in SGC7901 cells treated with EGB were determined using PCR and Western blot. And subcutaneous xenograft model of gastric carcinoma in nude mice was established to evaluate the anti-cancer effect of EGB in vivo.

RESULTS:

The proliferation of gastric carcinoma SGC7901 cells was inhibited by EGB in dose- and time-dependent manner. Flow cytometry showed cell cycle arrest in EGB-treated cells, with increased percentage of cells in G1 phase and decreased percentage in S stage. In addition, the mRNA and protein level of cyclin D1 and c-myc genes were significantly down-regulated in cells with EGB treatment with the concentration increasing.

CONCLUSION:

EGB conferred an inhibitory effect on the proliferation of gastric carcinoma SGC7901 cells both in vitro and in vivo. The inhibitory effect was dose dependent and possibly depended on inhibiting cell cycle through G1 arrest induction by suppressing cyclin D1 and c-myc expression.

KEYWORDS:

Cell proliferation; EGB; Gastric carcinoma

PMID:
26489423
DOI:
10.1007/s12094-015-1399-3
[Indexed for MEDLINE]

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