Zhu Xiaofeng, Zhu Ronghua
Department of Otorhinolaryngology, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450000, People's Republic of China.
Department of Otorhinolaryngology, Jinan Central Hospital Affiliated to Shandong University, Jinan 250013, People's Republic of China.
Onco Targets Ther. 2018 Jun 19;11:3521-3531. doi: 10.2147/OTT.S159236. eCollection 2018.
Curcumin is a polyphenol extracted from the rhizomes of with extensive biological and pharmacological effects. The present study aimed to investigate the mechanisms of curcumin in laryngeal squamous cell carcinoma (LSCC).
Quantitative real-time reverse transcriptase-polymerase chain reaction was performed to detect the expressions of miR-145 in LSCC tissues and cells. The effects of miR-145 and curcumin on cell proliferation, apoptosis, cell cycle, migration and invasion were explored by MTT assay, flow cytometry analysis, Transwell migration and invasion assay, respectively. The effects of miR-145 combined with curcumin on the phosphoinositol 1,3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway were detected by Western blot analysis.
miR-145 was significantly downregulated in LSCC tissues and cells. Curcumin administration upregulated miR-145 expression in LSCC cells in a dose-dependent manner. miR-145 overexpression and curcumin treatment both markedly suppressed cell proliferation, migration and invasion and induced cell cycle arrest and apoptosis in LSCC cells. Moreover, curcumin treatment reversed the enhanced effects on cell viability, migration and invasion and the inhibitory effects on apoptosis conferred by anti-miR-145 in LSCC cells. Curcumin treatment dramatically aggravated miR-145-induced inhibition of the PI3K/Akt/mTOR pathway and reversed anti-miR-145-mediated activation of the PI3K/Akt/mTOR pathway in LSCC cells.
Curcumin suppressed LSCC progression through the upregulation of miR-145 and inhibition of the PI3K/Akt/mTOR pathway.
姜黄素是从姜黄根茎中提取的一种多酚,具有广泛的生物学和药理作用。本研究旨在探讨姜黄素在喉鳞状细胞癌(LSCC)中的作用机制。
采用定量实时逆转录-聚合酶链反应检测LSCC组织和细胞中miR-145的表达。分别通过MTT法、流式细胞术分析、Transwell迁移和侵袭试验探讨miR-145和姜黄素对细胞增殖、凋亡、细胞周期、迁移和侵袭的影响。通过蛋白质印迹分析检测miR-145与姜黄素联合对磷酸肌醇1,3激酶(PI3K)/蛋白激酶B(Akt)/雷帕霉素哺乳动物靶蛋白(mTOR)通路的影响。
miR-145在LSCC组织和细胞中显著下调。姜黄素给药以剂量依赖性方式上调LSCC细胞中miR-145的表达。miR-145过表达和姜黄素处理均显著抑制LSCC细胞的增殖、迁移和侵袭,并诱导细胞周期停滞和凋亡。此外,姜黄素处理逆转了抗miR-145对LSCC细胞活力、迁移和侵袭的增强作用以及对凋亡的抑制作用。姜黄素处理显著加重了miR-145诱导的PI3K/Akt/mTOR通路抑制,并逆转了抗miR-145介导的LSCC细胞中PI3K/Akt/mTOR通路的激活。
姜黄素通过上调miR-145和抑制PI3K/Akt/mTOR通路抑制LSCC进展。