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葛根素通过KLF2/NOTCH1信号通路抑制甲状腺癌的发展。

Puerarin Inhibits the Development of Thyroid Cancer Through KLF2/NOTCH1 Signaling.

作者信息

Zhou Yanghong, Li Wei, Huang Hong

机构信息

Department of Traditional Chinese Medicine and Integrated Chinese and Western Medicine, Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University), 410006 Changsha, Hunan, China.

出版信息

Discov Med. 2025 May;37(196):894-903. doi: 10.24976/Discov.Med.202537196.79.

DOI:10.24976/Discov.Med.202537196.79
PMID:40415364
Abstract

BACKGROUND

Puerarin is the major bioactive ingredient extracted from Pueraria lobata. Puerarin has an antitumor effect on many kinds of cancer. Accordingly, the aim of this study was to investigate the effect and mechanism of puerarin on thyroid cancer (TC) proliferation and apoptosis.

METHODS

TC and normal thyroid cells experienced exposure to puerarin at 0, 10, 50, or 100 μg/mL. Impacts of short hairpin RNA of Kruppel-like factor 2 (sh), overexpression, and notch receptor 1 () overexpression on the malignant biological phenotypes of TC cells were gauged by cell function experiments. Quantification of KLF2, NOTCH1, B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), and Cleaved caspase 3 was completed using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analyses. and levels in TC were analyzed using the Encyclopedia of RNA Interactomes (ENCORI) project database. Through rescue experiments, whether the anti-tumor effect of puerarin on TC is realized via / axis was dissected.

RESULTS

Puerarin inhibited the malignant growth of TC cells by up-regulating , which was reversed by sh. was lowly expressed in TC. Notably, was negatively regulated by and was highly expressed in TC. overexpression abrogated overexpression-inhibited malignant growth of TC cells, which was manifested as increased cell proliferation and Bcl-2 as well as decreased cell apoptosis, Bax and Cleaved caspase 3.

CONCLUSION

Puerarin suppresses TC cell proliferation and apoptosis via the / axis.

摘要

背景

葛根素是从野葛中提取的主要生物活性成分。葛根素对多种癌症具有抗肿瘤作用。因此,本研究旨在探讨葛根素对甲状腺癌(TC)增殖和凋亡的影响及其机制。

方法

将TC细胞和正常甲状腺细胞分别暴露于0、10、50或100μg/mL的葛根素中。通过细胞功能实验评估Kruppel样因子2短发夹RNA(sh)、过表达以及Notch受体1()过表达对TC细胞恶性生物学表型的影响。使用定量实时聚合酶链反应(qRT-PCR)和蛋白质免疫印迹分析对KLF2、NOTCH1、B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)和裂解的半胱天冬酶3进行定量分析。利用RNA相互作用组百科全书(ENCORI)项目数据库分析TC中的和水平。通过挽救实验,剖析葛根素对TC的抗肿瘤作用是否通过/轴实现。

结果

葛根素通过上调抑制TC细胞的恶性生长,而sh可逆转这种作用。在TC中低表达。值得注意的是,受负调控且在TC中高表达。过表达消除了过表达抑制的TC细胞恶性生长,表现为细胞增殖增加、Bcl-2增加以及细胞凋亡、Bax和裂解的半胱天冬酶3减少。

结论

葛根素通过/轴抑制TC细胞增殖和凋亡。

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