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Updated: Jan 26, 2026

Intratibial Osteosarcoma Cell Injection to Generate Orthotopic Osteosarcoma and Lung Metastasis Mouse Models
Published on: October 28, 2021
STIM1 expression is associated with osteosarcoma cell survival
Jie Zang1,2, Dongqing Zuo1,3, Kristen L Shogren1
1Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN 55905, USA.
Objective:
To examine the role of store-operated calcium entry (SOCE) and stromal interaction molecule 1 (STIM1) in survival and migration of osteosarcoma cells and investigate what blockade of store-operated Ca2+ contributes to the regulation of osteosarcoma cells.
Methods:
First, we examined the expression levels of STIM1 in osteosarcoma cell lines by Western analysis and in tissue specimens by immunohistochemistry. Second, we investigated the effect of SOCE and STIM1 on osteosarcoma cell viability using MTS assays and on cell proliferation using colony formation. Third, we investigated the role of SOCE and STIM1 in cell migration using wound healing assays and Boyden chamber assays. Finally, we studied the effect of SOCE on the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) activity by luciferase assays.
Results:
STIM1 was overexpressed in osteosarcoma cell lines and tissue specimens and was associated with poor survival of osteosarcoma patients. Also, inhibition of SOCE and STIM1 decreased the cell viability and migration of osteosarcoma cells. Furthermore, our results showed that blockade of store-operated Ca2+ channels involved down-regulation of NFATc1 in osteosarcoma cells.
Conclusions:
STIM1 is essential for osteosarcoma cell functions, and STIM1 and Ca2+ entry pathway could be further explored as molecular targets in the treatment of osteosarcoma.
Insights
Stromal interaction molecule 1 (STIM1) is crucial for osteosarcoma cell survival and migration. Blocking store-operated calcium entry (SOCE) and STIM1 inhibits osteosarcoma progression, highlighting their potential as therapeutic targets.
Area of Science:
- Oncology
- Cell Biology
- Calcium Signaling
Background:
- Osteosarcoma is a primary bone malignancy with limited treatment options.
- Store-operated calcium entry (SOCE) and Stromal Interaction Molecule 1 (STIM1) are implicated in cancer cell functions.
- Understanding their role in osteosarcoma is critical for developing new therapies.
Purpose of the Study:
- To investigate the role of SOCE and STIM1 in osteosarcoma cell survival and migration.
- To determine the effect of blocking SOCE and STIM1 on osteosarcoma progression.
- To explore the downstream signaling pathways regulated by SOCE in osteosarcoma.
Main Methods:
- Western blot and immunohistochemistry to assess STIM1 expression in osteosarcoma cells and tissues.
- MTS assays and colony formation assays to evaluate cell viability and proliferation.
- Wound healing and Boyden chamber assays to analyze cell migration.
- Luciferase assays to measure NFATc1 activity.
Main Results:
- STIM1 was overexpressed in osteosarcoma cell lines and patient tissues, correlating with poor survival.
- Inhibition of SOCE and STIM1 significantly reduced osteosarcoma cell viability and migration.
- Blocking store-operated calcium channels led to the down-regulation of NFATc1 in osteosarcoma cells.
Conclusions:
- STIM1 plays an essential role in the survival and migration of osteosarcoma cells.
- The STIM1 and SOCE pathway represents a promising molecular target for osteosarcoma treatment.
- Targeting calcium entry could offer a novel therapeutic strategy for osteosarcoma.
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