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Updated: Jan 27, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
Elevated expression of microRNA-328-3p suppresses aggressive malignant behaviors via targeting matrix metalloprotease
Ming Zhang1, Jiayuan Zhang1, Quan Zhou1
1Department of Orthopaedics, Huai'an Hospital Affiliated to Xuzhou Medical College and Huai'an Second Hospital, Huai'an, Jiangsu, People's Republic of China, wuque197928@163.com.
Background:
A previous study indicated that microRNA(miR)-328-3p upregulation might be critical for resveratrol-mediated suppression of metastatic ability in human osteosarcoma, implying its potential role in this malignancy. However, the clinical significance and the biological functions of miR-328-3p in osteosarcoma remain unclear.
Methods:
miR-328-3p expression in 88 pairs of osteosarcoma and matched non-cancerous bone tissues were detected by quantitative real-time PCR. Then, the associations of miR-328-3p expression with various clinicopathological features of osteosarcoma patients were statistically analyzed. Cell Counting Kit-8 and scratch-wound healing were performed to evaluate roles of miR-328-3p in human osteosarcoma cells. After that, luciferase reporter assay, western blot analysis and rescue assay were applied to determine the underlying molecular mechanisms of miR-328-3p in osteosarcoma cells.
Results:
miR-328-3p expression in osteosarcoma tissues was significantly lower than those in non-cancerous bone tissues (P<0.001). miR-328-3p downregulation was significantly associated with advanced surgical stage, positive metastasis and recurrence (all P<0.05). Functionally, enforced expression of miR-328-3p efficiently suppressed cell proliferation and migration in vitro. Moreover, matrix metalloprotease 16 (MMP16) was identified as a direct target of miR-328-3p in osteosarcoma cells. Notably, MMP16 overexpression partially reversed the miR-328-3p-inhibited cell proliferation and migration of osteosarcoma cells.
Conclusions:
Our data indicated that the aberrant expression of miR-328-3p may play a crucial role in malignant progression of human osteosarcoma. More importantly, miR-328-3p may function as a tumor suppressor inhibiting osteosarcoma cell proliferation and migration partially mediated by regulating of MMP16.
Insights
MicroRNA-328-3p is downregulated in osteosarcoma, suppressing tumor growth and metastasis. Its regulation of MMP16 highlights its potential as a therapeutic target for osteosarcoma progression.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Previous research suggested microRNA (miR)-328-3p upregulation inhibits metastasis in osteosarcoma.
- The clinical relevance and specific functions of miR-328-3p in osteosarcoma were previously undetermined.
Purpose of the Study:
- To investigate the clinical significance and biological roles of miR-328-3p in human osteosarcoma.
- To elucidate the molecular mechanisms underlying miR-328-3p's function in osteosarcoma progression.
Main Methods:
- Quantitative real-time PCR to measure miR-328-3p expression in osteosarcoma tissues.
- Statistical analysis of miR-328-3p expression with clinicopathological features.
- In vitro assays (Cell Counting Kit-8, scratch-wound healing) to assess miR-328-3p's functional impact.
- Luciferase reporter assay, western blot, and rescue assays to identify molecular targets and mechanisms.
Main Results:
- miR-328-3p expression was significantly lower in osteosarcoma tissues compared to non-cancerous bone.
- Downregulation of miR-328-3p correlated with advanced stage, metastasis, and recurrence.
- Enforced miR-328-3p expression inhibited osteosarcoma cell proliferation and migration.
- Matrix metalloprotease 16 (MMP16) was identified as a direct target, and its overexpression partially reversed miR-328-3p's inhibitory effects.
Conclusions:
- Aberrant miR-328-3p expression is linked to malignant progression in human osteosarcoma.
- miR-328-3p acts as a tumor suppressor by inhibiting cell proliferation and migration.
- The tumor-suppressive function of miR-328-3p is partially mediated through the regulation of MMP16.
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