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Updated: Mar 28, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
Published on: April 12, 2019
Downregulation of connective tissue growth factor reduces migration and invasiveness of osteosarcoma cells
Yinjun Huang1, Shichang Zhao1, Changqing Zhang1
1Department of Orthopedic Surgery, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai 200233, P.R. China.
Abstract:
As one of the most serious types of primary bone tumor, osteosarcoma (OSA) features metastatic lesions, and resistance to chemotherapy is common. The underlying mechanisms of these characteristics may account for the failure of treatments and the poor prognosis of patients with OSA. It has been reported that inhibition of Cyr61 suppresses OSA cell proliferation as it represents a target of statins. In addition to cystein‑rich protein 61 (Cyr61) and nephroblastoma overexpression, connective tissue growth factor (CTGF) is a member of the CCN family and may therefore exhibit effects on human OSA cells similar to those of Cyr61. In the current study, acridine orange/ethidium bromide staining were used to determine the rate of apoptosis. The present study demonstrated that small interfering RNA‑mediated silencing of CTGF promoted cell death and suppressed OSA cell migration and invasion, as indicated by wound healing and Transwell assays, while lentivirus‑mediated overexpression of CTGF reversed these effects. Furthermore, a colorimetric caspase assay demonstrated that CTGF knockdown enhanced the efficacy of chemotherapeutic drugs. The results of the present study provided a novel molecular target which may be utilized for the treatment of metastatic OSA.
Insights
Connective tissue growth factor (CTGF) silencing promotes osteosarcoma (OSA) cell death and migration inhibition. CTGF knockdown also enhances chemotherapy efficacy, offering a potential new target for metastatic OSA treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Osteosarcoma (OSA) is a primary bone tumor characterized by metastasis and chemotherapy resistance, leading to poor patient prognosis.
- Connective tissue growth factor (CTGF), a member of the CCN family, is implicated in cellular processes relevant to OSA.
- Understanding CTGF's role may reveal new therapeutic targets for overcoming OSA treatment failures.
Purpose of the Study:
- To investigate the role of CTGF in osteosarcoma (OSA) cell behavior, including proliferation, apoptosis, migration, and invasion.
- To evaluate the potential of CTGF as a therapeutic target for metastatic OSA.
- To determine if modulating CTGF affects the efficacy of chemotherapeutic drugs in OSA.
Main Methods:
- Small interfering RNA (siRNA) was used to silence CTGF expression in OSA cells.
- Lentivirus-mediated gene delivery was employed for CTGF overexpression.
- Cell apoptosis was assessed using acridine orange/ethidium bromide staining.
- Cell migration and invasion were evaluated through wound healing and Transwell assays.
- Caspase activity was measured using a colorimetric assay to assess drug efficacy.
Main Results:
- CTGF silencing significantly promoted cell death and suppressed OSA cell migration and invasion.
- Overexpression of CTGF reversed the effects observed upon silencing.
- Knockdown of CTGF enhanced the efficacy of standard chemotherapeutic drugs.
- These findings identify CTGF as a key regulator of OSA progression and chemosensitivity.
Conclusions:
- CTGF plays a crucial role in promoting osteosarcoma cell survival, migration, and invasion.
- Silencing CTGF presents a promising strategy to inhibit OSA progression and metastasis.
- Targeting CTGF may enhance the effectiveness of chemotherapy, offering a novel therapeutic approach for metastatic osteosarcoma.
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