Licochalcone A inhibits cell proliferation, migration, and invasion through regulating the PI3K/AKT signaling pathway in oral squamous cell carcinoma
Authors Hao Y, Zhang C, Sun Y, Xu H
Received 17 January 2019
Accepted for publication 26 April 2019
Published 5 June 2019 Volume 2019:12 Pages 4427—4435
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Ms Rachel Predeepa
Peer reviewer comments 4
Editor who approved publication: Dr William Cho
Yuli Hao,1,* Chunping Zhang,1,* Yuanyuan Sun,2 Hongyan Xu3
1Department of Stomatology, Yuhuangding Hospital, Yantai 264000, People’s Republic of China; 2Department of Periodontology, Yantai Stomatological Hospital, Yantai 264000, People’s Republic of China; 3Department of Stomatology, Shaanxi People’s Hospital, Xian 710000, People’s Republic of China
*These authors contributed equally to this work
Background: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, with high metastasis and mortality. Licochalcone A (LCA) is a chalconoid from the root of Glycyrrhiza inflata, which has anti-tumor, anti-inflammatory, anti-angiogenesis effects in many cancers. However, the mechanism that underlies LCA regulating cell proliferation, migration, and invasion in OSCC remains poorly understood.
Methods: LY294002 or insulin-like growth factor 1 (IGF-1) were used to block or stimulate the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathway in OSCC cells. Cell proliferation was investigated by MTT assay and proliferating cell nuclear antigen (PCNA) protein level using Western blot. The expression of metastasis-related protein was detected via Western blot. Cell migration and invasion abilities were evaluated by trans-well assay. A murine xenograft model of OSCC was established to investigate the anti-tumor effect of LCA in vivo.
Results: Treatment of LCA inhibited cell proliferation in SCC4 and CAL-27 cells. Moreover, PI3K/AKT signaling was blocked by LY294002, and activated by IGF-1. LCA could suppress proliferation, migration, and invasion of OSCC cells, which was similar to the treatment of LY294002. In addition, LCA decreased IGF-1-induced OSCC progression. In a murine xenograft model, LCA treatment protected against tumor growth and metastasis in vivo.
Conclusions: LCA might inhibit cell proliferation, migration, and invasion through regulating the PI3K/AKT pathway in OSCC, developing a potential chemotherapeutic agent for OSCC.
Keywords: oral squamous cell carcinoma, Licochalcone A, PI3K/AKT, PCNA, migration, invasion
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