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Published on: June 13, 2019
Deficiency of TTYH1 Expression Reduces the Migration and Invasion of U2OS Human Osteosarcoma Cells
Young-Sun Lee1,2, Osung Kwon1, Geuk-Rae Jeong1
1School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Korea.
Abstract:
The Tweety homolog (TTYH) chloride channel family is involved in oncogenic processes including cell proliferation, invasion, and colonization of cancers. Among the TTYH family, TTYH1 is highly expressed in several cancer cells, such as glioma, breast, and gastric cancer cells. However, the role of TTYH1 in the progression of osteosarcoma remains unknown. Here, we report that deficient TTYH1 expression results in the inhibition of the migration and invasion of U2OS human osteosarcoma cells. We found that TTYH1 was endogenously expressed at both mRNA and protein levels in U2OS cells and that these channels were located at the plasma membrane of the cells. Moreover, we found that silencing of the TTYH1 with small interfering RNA (siRNA) resulted in a decrease in the migration and invasion of U2OS cells, while the proliferation of the cells was not affected. Additionally, treatment with TTYH1 siRNA significantly suppressed the mRNA expression of epithelial−mesenchymal transition (EMT)-regulated transcription factors such as Zinc E-Box Binding Homeobox 1 (ZEB1) and SNAIL. Most importantly, the expression of matrix metalloproteinase (MMP)-2, MPP-9, and N-cadherin was dramatically reduced following the silencing of TTYH1. Taken together, our findings suggest that silencing of TTYH1 expression reduces migration and invasion of U2OS cells and that TTYH1 may act as a potential molecular target for osteosarcoma treatment.
Insights
Tweety homolog 1 (TTYH1) silencing inhibits osteosarcoma cell migration and invasion without affecting proliferation. TTYH1 may be a therapeutic target for osteosarcoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- The Tweety homolog (TTYH) chloride channel family, particularly TTYH1, is implicated in cancer progression.
- TTYH1 is overexpressed in glioma, breast, and gastric cancers, but its role in osteosarcoma is unknown.
Purpose of the Study:
- To investigate the role of TTYH1 in the progression of U2OS human osteosarcoma cells.
- To determine if TTYH1 could be a potential therapeutic target for osteosarcoma.
Main Methods:
- Endogenous TTYH1 expression and localization in U2OS cells were assessed.
- TTYH1 was silenced using small interfering RNA (siRNA).
- Cell migration, invasion, and proliferation assays were performed. Expression of epithelial-mesenchymal transition (EMT) markers and matrix metalloproteinases (MMPs) was analyzed.
Main Results:
- TTYH1 is endogenously expressed at mRNA and protein levels in U2OS cells and localized to the plasma membrane.
- Silencing TTYH1 significantly reduced U2OS cell migration and invasion but did not affect proliferation.
- TTYH1 silencing suppressed the expression of EMT transcription factors (ZEB1, SNAIL) and MMPs (MMP-2, MMP-9), and N-cadherin.
Conclusions:
- TTYH1 silencing inhibits osteosarcoma cell migration and invasion.
- TTYH1 plays a role in osteosarcoma progression and represents a potential molecular target for treatment.
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