Peptide P11 suppresses the growth of human thyroid carcinoma by inhibiting the PI3K/AKT/mTOR signaling pathway

被引:0
作者
Dongdong Wu
Wenke Tian
Jianmei Li
Qianqian Zhang
Honggang Wang
Lei Zhang
Zhongwen Xie
Ailing Ji
Yanzhang Li
机构
[1] Henan University,School of Basic Medical Sciences
[2] Henan University,Joint National Laboratory for Antibody Drug Engineering, Henan International Joint Laboratory for Nuclear Protein Regulation
[3] Anhui Agricultural University,State Key Laboratory of Tea Plant Biology and Utilization
来源
Molecular Biology Reports | 2019年 / 46卷
关键词
Peptide P11; Thyroid carcinoma; Apoptosis; Signaling pathway;
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学科分类号
摘要
Thyroid carcinoma is the most common endocrine malignancy, and the incidence of thyroid carcinoma is increasing in recent decades. CYYGQSKYC (P6), a nonapeptide with anti-lymphangiogenic effect by its binding to VEGFR-3 and selectively inhibiting VEGF-C binding to VEGFR-3, could suppress the migration and invasion of cancer cells. LSPPRYP (P9) acts as an effective bFGF/FGFR antagonist and inhibits the growth of the murine melanoma B16-F10 cells. In order to increase the anti-tumor effects of P6 and P9, we connected P6 with P9 via a flexible linker Gly-Gly-Gly (GGG) to reconstruct a novel peptide P11, CYYGQSKYCGGGLSPPRYP. In the present study, the mechanism of action of peptide P11 on the growth of human thyroid carcinoma cells both in vitro and in vivo was determined. Our results showed that peptide P11 inhibited the proliferation, viability, migration, and invasion of human thyroid carcinoma cells. Peptide P11 increased the apoptosis and decreased the protein levels of p-PI3K, p-AKT, and p-mTOR in human thyroid carcinoma cells. In addition, P11 could effectively inhibit the growth of human thyroid carcinoma xenograft tumors in nude mice. In conclusion, peptide P11 could inhibit the growth of human thyroid carcinoma by inhibiting the PI3K/Akt/mTOR signaling pathway. Novel peptides can be designed and applied for the treatment of various types of cancer.
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页码:2665 / 2678
页数:13
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