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雷公藤内酯醇通过星形胶质细胞上调基因-1抑制甲状腺癌细胞的转移潜能。

Triptonide inhibits metastasis potential of thyroid cancer cells via astrocyte elevated gene-1.

作者信息

Fu Liangjie, Niu Xiaohong, Jin Ruhui, Xu Feiyun, Ding Jiguo, Zhang Li, Huang Zihui

机构信息

Department of Scrofulosis, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing 210014, China.

出版信息

Transl Cancer Res. 2020 Feb;9(2):1195-1204. doi: 10.21037/tcr.2019.12.94.

DOI:10.21037/tcr.2019.12.94
PMID:35117464
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8799231/
Abstract

BACKGROUND

Triptonide (TN) was recently proved to have anti-tumor effects. The current study explored whether TN inhibited thyroid cancer and the possible underlying mechanism.

METHODS

MDA-T68 and BCPAP cells were treated by TN. Cell viability, migration and invasion rate were detected by MTT and Transwell. Protein expressions were determined by Western blot and mRNA expressions were detected by Real-time Quantitative PCR (qPCR).

RESULTS

TN at the concentration higher than 50 nmol/L inhibited cell viability, migration and invasion of MDA-T68 and BCPAP cells, and astrocyte elevated gene (AEG-1) expression, was decreased by TN at the concentration higher than 50 nmol/L. Furthermore, overexpression inhibited cell viability, migration and invasion capacity of MDA-T68 and BCPAP cells, while TN reduced AEG-1 expression, and weaken the effect of overexpression on cell viability, migration and invasion capacities. Moreover, TN depressed the increase of matrix metalloproteinase (MMP) 2, MMP9 and N-cadherin expressions caused by AEG-1 overexpression. Meanwhile, E-cadherin expression reduced by AEG-1 overexpression was increased by TN.

CONCLUSIONS

TN could inhibit the metastasis potential of thyroid cancer cells through inhibiting the expression of AEG-1. Our findings reveal the mechanism of TN in the treatment of thyroid cancer, which should be further explored in the study of thyroid cancer.

KEYWORDS

Triptonide; metastasis; thyroid cancer; regulation; drug monomer.

摘要

背景

雷公藤甲素（TN）最近被证明具有抗肿瘤作用。本研究探讨TN是否能抑制甲状腺癌及其可能的潜在机制。

方法

用TN处理MDA-T68和BCPAP细胞。通过MTT和Transwell检测细胞活力、迁移和侵袭率。通过蛋白质印迹法测定蛋白质表达，通过实时定量PCR（qPCR）检测mRNA表达。

结果

浓度高于50 nmol/L的TN抑制MDA-T68和BCPAP细胞的活力、迁移和侵袭，且浓度高于50 nmol/L的TN可降低星形细胞升高基因（AEG-1）的表达。此外，过表达抑制MDA-T68和BCPAP细胞的活力、迁移和侵袭能力，而TN降低AEG-1表达，并减弱过表达对细胞活力、迁移和侵袭能力的影响。此外，TN抑制了由AEG-1过表达引起的基质金属蛋白酶（MMP）2、MMP9和N-钙黏蛋白表达的增加。同时，TN增加了因AEG-1过表达而降低的E-钙黏蛋白表达。

结论

TN可通过抑制AEG-1的表达来抑制甲状腺癌细胞的转移潜能。我们的研究结果揭示了TN治疗甲状腺癌的机制，这在甲状腺癌研究中应进一步探索。

关键词

雷公藤甲素；转移；甲状腺癌；调控；药物单体

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/e18c7a85dda4/tcr-09-02-1195-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/21f1d70adee5/tcr-09-02-1195-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/0fd1ea18e0ba/tcr-09-02-1195-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/62dab5ef9357/tcr-09-02-1195-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/e18c7a85dda4/tcr-09-02-1195-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/21f1d70adee5/tcr-09-02-1195-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/0fd1ea18e0ba/tcr-09-02-1195-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/62dab5ef9357/tcr-09-02-1195-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/009b/8799231/e18c7a85dda4/tcr-09-02-1195-f4.jpg

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