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厚朴酚通过抑制 NF-κB 信号通路抑制胆管癌细胞的增殖和侵袭。

Magnolol suppresses the proliferation and invasion of cholangiocarcinoma cells via inhibiting the NF-κB signaling pathway.

机构信息

Xiamen Maternity and Child Health Care Hospital, Xiamen 361003, Fujian Province, China.

Department of Pathology, The Affiliated Southeast Hospital of Xiamen University, Zhangzhou 363000, Fujian Province, China.

出版信息

Biomed Pharmacother. 2017 Oct;94:474-480. doi: 10.1016/j.biopha.2017.07.085. Epub 2017 Aug 3.

DOI:10.1016/j.biopha.2017.07.085
PMID:28779709
Abstract

BACKGROUND

Magnolol has shown the potential anticancer properties against a variety of cancers. However, the role of magnolol in cholangiocarcinoma (CCA) cells is unknown. In this study, we assessed the effect of magnolol on the CCA cells.

METHODS

CCA cells were treated with magnolol in the absence or presence of TNFα, the activator for NF-κB. After co-incubation with magnolol, cell proliferation and growth were examined by MTT, colony formation and xenograft tumors; cell cycle was analyzed by flow cytometry; cell migration and invasion were detected by wound healing and transwell assays; the expression of PCNA, Ki67, CyclinD1, MMP-2, MMP-7 and MMP-9 and NF-κB pathway were evaluated by using Western blot.

RESULTS

Magnolol inhibited the abilities of CCA cell growth, migration and invasion accompanying with a decreased expression of PCNA, Ki67, MMP-2, MMP-7 and MMP-9 (all P<0.05).

TREATMENT

with magnolol induced cell cycle arrest in G1 phase with a downregulation of cell cycle protein CyclinD1 (all P<0.05). In addition, magnolol suppressed the expression of p-IκBα and p-P65 and the effect of magnolol on CCA cells could be inhibited by TNFα.

CONCLUSIONS

Magnolol could inhibit the growth, migration and invasion of CCA cells through regulation of NF-κB pathway, and these data indicate that magnolol is a potential candidate for treating of CCA.

摘要

背景

厚朴酚已显示出对多种癌症具有潜在的抗癌特性。然而,厚朴酚在胆管癌(CCA)细胞中的作用尚不清楚。在这项研究中,我们评估了厚朴酚对 CCA 细胞的作用。

方法

在不存在或存在 TNFα(NF-κB 的激活剂)的情况下,用厚朴酚处理 CCA 细胞。与厚朴酚共孵育后,通过 MTT、集落形成和异种移植肿瘤检测细胞增殖和生长;通过流式细胞术分析细胞周期;通过划痕愈合和 Transwell 测定检测细胞迁移和侵袭;通过 Western blot 评估 PCNA、Ki67、CyclinD1、MMP-2、MMP-7 和 MMP-9 的表达和 NF-κB 通路。

结果

厚朴酚抑制 CCA 细胞生长、迁移和侵袭的能力,伴随 PCNA、Ki67、MMP-2、MMP-7 和 MMP-9 的表达降低(均 P<0.05)。

治疗

厚朴酚诱导细胞周期停滞在 G1 期,细胞周期蛋白 CyclinD1 下调(均 P<0.05)。此外,厚朴酚抑制 p-IκBα 和 p-P65 的表达,TNFα 可抑制厚朴酚对 CCA 细胞的作用。

结论

厚朴酚可通过调节 NF-κB 通路抑制 CCA 细胞的生长、迁移和侵袭,这些数据表明厚朴酚是治疗 CCA 的潜在候选药物。

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