4.7 Article

Pentagalloylglucose suppresses the growth and migration of human nasopharyngeal cancer cells via the GSK3β/β-catenin pathway in vitro and in vivo

期刊

PHYTOMEDICINE
卷 102, 期 -, 页码 -

出版社

ELSEVIER GMBH
DOI: 10.1016/j.phymed.2022.154192

关键词

Nasopharyngeal carcinoma; Pentagalloylglucose; Migration; Autophagy; Wnt/beta-catenin pathway

资金

  1. National Natural Science Foundation of China [21977021, 81760626, 22111530012]
  2. Natural Science Foundation of Guangxi Province [AB17292075]
  3. Open Funds of the Guangxi Key Laboratory of tumor Immunology and Microenvironmental Regulation [2018KF002]
  4. Guangxi Funds for Distinguished Experts

向作者/读者索取更多资源

This study demonstrated that PGG can inhibit proliferation, induce apoptosis and autophagy, and decrease metastatic capacity of NPC cells. Mechanistically, PGG exerts its effects through the p38 MAPK/mTOR and Wnt/beta-catenin pathways, providing evidence for PGG as a potential therapeutic option for NPC.
Background: Nasopharyngeal carcinoma (NPC) is a type of malignant squamous cell tumour originating from the nasopharynx epithelium. Pentagalloylglucose (PGG) is a natural polyphenolic compound that exerts anticancer effects in many types of tumours. However, the role and underlying mechanism of PGG in NPC cells have not been fully defined. Purpose: This study aimed to investigate the anticancer activity of PGG as well as the potential mechanism in NPC cells. Methods: The effects of PGG on the proliferation, apoptosis and cell cycle distribution of CNE1 and CNE2 cells were assessed by MTT and flow cytometry assays. Cell migration was evaluated using wound healing and transwell assays. The expression of microtubule-associated protein 1 light chain 3 beta (LC3B) was observed by immunofluorescence staining. Western blotting was used to explore the levels of related proteins and signalling pathway components. Furthermore, the effects of PGG on NPC cell growth were analysed in a xenograft mouse model in vivo using cisplatin as a positive control. Results: PGG dose-dependently inhibited the proliferation of CNE1 and CNE2 cells. PGG regulated the cell cycle by altering p53, cyclin D1, CDK2, and cyclin E1 protein levels. PGG induced apoptosis and autophagy in NPC cells and elevated the Bax/Bcl-2 ratio and the protein levels of LC3B. Moreover, PGG decreased NPC cell migration by increasing E-cadherin and decreasing N-cadherin, vimentin and CD44 protein levels. Mechanistically, PGG treatment downregulated p-mTOR and beta-catenin expression but upregulated p-p38 MAPK and pGSK3 beta expression. In addition, PGG significantly inhibited NPC cell tumour growth and lung metastasis in vivo. Conclusion: PGG may suppress cell proliferation, induce apoptosis and autophagy, and decrease the metastatic capacity of NPC cells through the p38 MAPK/mTOR and Wnt/beta-catenin pathways. The present study provides evidence for PGG as a potential therapy for NPC.

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