Triptonide inhibits metastasis potential of thyroid cancer cells via astrocyte elevated gene-1
Liangjie Fu1, Xiaohong Niu1, Ruhui Jin1
1Department of Scrofulosis, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Nanjing 210014, China.
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, AEG-1 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 AEG-1 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.
Insights
Triptonide (TN) inhibits thyroid cancer metastasis by reducing astrocyte elevated gene (AEG-1) expression. This study reveals TN
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Triptonide (TN) has demonstrated anti-tumor properties.
- The role of TN in thyroid cancer progression and its underlying mechanisms require elucidation.
- Thyroid cancer metastasis is a significant clinical challenge.
Purpose of the Study:
- To investigate the inhibitory effects of Triptonide (TN) on thyroid cancer.
- To explore the molecular mechanisms by which TN affects thyroid cancer cell behavior.
- To determine the role of astrocyte elevated gene (AEG-1) in TN's anti-cancer activity.
Main Methods:
- Thyroid cancer cell lines (MDA-T68 and BCPAP) were treated with TN.
- Cell viability, migration, and invasion were assessed using MTT and Transwell assays.
- Protein and mRNA expression levels of key genes, including AEG-1, MMPs, and cadherins, were analyzed via Western blot and qPCR.
Main Results:
- Triptonide (TN) significantly inhibited thyroid cancer cell viability, migration, and invasion at concentrations above 50 nmol/L.
- TN treatment led to a decrease in astrocyte elevated gene (AEG-1) expression.
- Overexpression of AEG-1 promoted cancer cell proliferation and metastasis, effects that were attenuated by TN, which also reversed AEG-1-induced changes in MMPs and cadherins.
Conclusions:
- Triptonide (TN) effectively inhibits the metastatic potential of thyroid cancer cells.
- The mechanism involves the downregulation of astrocyte elevated gene (AEG-1) expression.
- These findings highlight TN as a potential therapeutic agent for thyroid cancer, warranting further investigation.
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