Related Experiment Video
Updated: May 17, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
SASH1 regulates proliferation, apoptosis, and invasion of osteosarcoma cell
Qingbing Meng1, Minqian Zheng, Hongbing Liu
1Orthopedics Department, Yancheng City No. 1 People's Hospital, 16 Yue-He Road, Yancheng 224005, Jiangsu, People's Republic of China. ycmengqingbing@163.com
Abstract:
SASH1, a member of the SLY-family of signal adapter proteins, is a candidate tumor suppressor in breast and colon cancer. The SASH1 protein possesses both the SH3 and SAM domains, indicating that it may play an important role in intracellular signal transduction. Reduced expression of SASH1 is closely related to tumor growth, invasion, metastasis, and poor prognosis. However, the biological role of SASH1 remains unknown in osteosarcoma. To unravel the function of SASH1, we explored the expression of SASH1 in osteosarcoma tissues and its correlation to the clinical pathology of osteosarcoma and analyzed the relationship between SASH1 expression and cell cycle, apoptosis and invasion of osteosarcoma MG-63 cells, using the flow cytometry analysis and transwell invasion chamber experiments. Furthermore, the effect of SASH1 on the expression of cyclin D1, caspase-3, matrix metalloproteinase (MMP)-9 were observed by western blot. Our results showed that the expression rate of SASH1 mRNA in osteosarcoma tissues was significantly lower than that in normal bone tissue (p = 0.000), that the expression rate of SASH1 mRNA in the carcinoma tissues from patients with lung metastasis was significantly lower than that from patients without lung metastasis (p = 0.041), and that the expression rate of SASH1 mRNA also decreased with increasing Enneking stage (p = 0.032). However, the mRNA expression of SASH1 in osteosarcoma was independent of the patient's gender, age, and tumor size (p = 0.983, 0.343, 0.517, respectively). The SASH1 protein displayed a down-regulation in osteosarcoma tissues compared to normal bone tissue (p = 0.000), displayed a down-regulation in osteosarcoma tissues from patients with lung metastasis compared to from patients without lung metastasis (p = 0.000), and displayed a gradual decrease with increasing Enneking stage (p = 0.000). In addition, the MG-63 cells from pcDNA3.1-SASH1 group exhibited significantly reduced cell viability, proliferation, and invasive ability compared to the empty vector group and blank control group (p = 0.023, 0.001, respectively), and there was no difference between the empty vector group and blank control group. The pcDNA3.1-SASH1 group displayed significantly more apoptotic cells than the empty vector group and blank control group (p = 0.004). The expression of cyclin D1, MMP-9 displayed a down-regulation in MG-63 cells from pcDNA3.1-SASH1 group compared to the empty vector group and blank control group (p = 0.000, 0.001, respectively) and the expression levels of caspase-3 displayed an up-regulation in MG-63 cells from pcDNA3.1-SASH1 group compared to the empty vector group and blank control group (p = 0.000). Taken together, these data indicated that the overexpression of SASH1 might be associated with the inhibition of growth, proliferation, and invasion of MG-63 cells and the promotion of apoptosis of MG-63 cells.
Insights
The SASH1 protein, a potential tumor suppressor, is significantly downregulated in osteosarcoma, correlating with increased metastasis and poorer prognosis. Overexpressing SASH1 inhibits osteosarcoma cell growth, invasion, and promotes apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- SASH1 (SAM and SH3 domain-containing protein 1) is a candidate tumor suppressor implicated in breast and colon cancers.
- Reduced SASH1 expression is linked to tumor progression, invasion, metastasis, and poor patient outcomes.
- The specific role of SASH1 in osteosarcoma pathogenesis remained largely unexplored.
Purpose of the Study:
- To investigate the expression patterns of SASH1 in osteosarcoma tissues.
- To correlate SASH1 expression with clinical-pathological features of osteosarcoma.
- To elucidate the functional role of SASH1 in osteosarcoma cell behavior, including proliferation, apoptosis, and invasion.
Main Methods:
- Quantitative analysis of SASH1 mRNA and protein expression in osteosarcoma tissues versus normal bone.
- Correlation analysis between SASH1 expression levels and clinical parameters (metastasis, Enneking stage, gender, age, tumor size).
- In vitro experiments using MG-63 osteosarcoma cells to assess the effects of SASH1 overexpression on cell viability, proliferation, apoptosis, and invasion, alongside Western blot analysis for key regulatory proteins (cyclin D1, caspase-3, MMP-9).
Main Results:
- SASH1 mRNA and protein expression were significantly downregulated in osteosarcoma tissues compared to normal bone.
- Lower SASH1 expression correlated with lung metastasis and advanced Enneking stage, but not with gender, age, or tumor size.
- Overexpression of SASH1 in MG-63 cells led to reduced cell viability, proliferation, and invasion, increased apoptosis, and altered expression of cyclin D1, caspase-3, and MMP-9.
Conclusions:
- SASH1 functions as a tumor suppressor in osteosarcoma.
- Downregulation of SASH1 is associated with aggressive osteosarcoma phenotypes and poor prognosis.
- SASH1 overexpression exhibits anti-tumor effects by inhibiting proliferation and invasion while promoting apoptosis in osteosarcoma cells.
Related Concept Videos
Abnormal Proliferation
The JAK-STAT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
Inhibition of Cdk Activity

