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Fingolimod inhibits proliferation and epithelial-mesenchymal transition in sacral chordoma by inactivating IL-6/STAT3
Jiaqi Wang1, Wenhao Hu2, Xiaowen Du1
1Department of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110000, China.
Purpose:
To explore the sensitivity of the immunosuppressive agent fingolimod (FTY720) in chordoma and determine whether it can serve as an appropriate alternate treatment for unresectable tumours in patients after incomplete surgery.
Methods:
Cell viability assays, colony formation assays and EdU assays were performed to evaluate the sensitivity of chordoma cell lines to FTY720. Transwell invasion assays, wound healing assays, flow cytometry, cell cycle analysis, immunofluorescence analysis, Western blotting analysis and enzyme-linked immunosorbent assays (ELISAs) were performed to evaluate cell invasion, epithelial-mesenchymal transition (EMT) and activation of related pathways after treatment with FTY720. The effect of FTY720 was also evaluated in vivo in a xenograft model.
Results:
We found that FTY720 inhibited the proliferation, invasion and metastasis of sacral chordoma cells (P < 0.01). FTY720 also inhibited the proliferation of tumour cells in a xenograft model using sacral chordoma cell lines (P < 0.01). The mechanism was related to the EMT and apoptosis of chordoma cells and inactivation of IL-6/STAT3 signalling in vitro and in vivo.
Conclusions:
Our findings indicate that FTY720 may be an effective therapeutic agent against chordoma. These findings suggest that FTY720 is a novel agent that can treat locally advanced and metastatic chordoma.
Insights
Fingolimod (FTY720) effectively inhibits chordoma cell proliferation, invasion, and metastasis. This immunosuppressive agent shows promise as a novel treatment for locally advanced and metastatic chordoma.
Area of Science:
- Oncology
- Immunology
- Pharmacology
Background:
- Chordoma is a rare bone tumor.
- Unresectable chordoma poses treatment challenges.
- Immunosuppressive agents are being explored for cancer therapy.
Purpose of the Study:
- To assess fingolimod's (FTY720) efficacy in chordoma.
- To evaluate FTY720 as an alternative treatment for unresectable chordoma post-surgery.
Main Methods:
- In vitro studies: cell viability, colony formation, EdU assays on chordoma cell lines.
- In vitro studies: invasion, wound healing, flow cytometry, cell cycle, immunofluorescence, Western blotting, ELISAs.
- In vivo studies: xenograft model using sacral chordoma cell lines.
Main Results:
- FTY720 significantly inhibited proliferation, invasion, and metastasis of sacral chordoma cells (P < 0.01).
- FTY720 suppressed tumor cell proliferation in a xenograft model (P < 0.01).
- Mechanisms involved epithelial-mesenchymal transition (EMT), apoptosis, and IL-6/STAT3 pathway inactivation.
Conclusions:
- FTY720 demonstrates potential as an effective therapeutic agent for chordoma.
- FTY720 may represent a novel treatment for locally advanced and metastatic chordoma.
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