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DEAD-Box Helicase 5 Interacts With Transcription Factor 12 and Promotes the Progression of Osteosarcoma by
Yanchun Chen1, Qiaozhen Wang2, Qing Wang2
1Department of Histology and Embryology, School of Clinical Medicine, Weifang Medical University, Weifang, China.
Abstract:
Osteosarcoma (OS) is a common malignant primary bone tumor. Its mechanism of development and progression is poorly understood. Currently, there is no effective therapeutic regimens available for the treatment of OS. DEAD-box helicase 5 (DDX5) is involved in oncogenic processes. This study aimed to explore the role of DDX5 in the development and progression of OS and its relationship with transcription factor 12 (TCF12), which is as an important molecule of Wnt signaling pathway. We found that the expressions of DDX5 and TCF12 protein were significantly higher in OS patients tissues and in the MG63 cells than in the corresponding normal tissues and human osteoblast cell hFOB 1.19. Overexpressions of both DDX5 and TCF12 were associated with clinicopathological features and poor prognosis of OS patients. siRNA based knockdown of DDX5 inhibited the proliferation of MG63 cells as demonstrated by an in vitro MTS assay and 5-ethynyl-2-deoxyuridine DNA proliferation detection, and promoted apoptosis of MG63 cells measured by flow cytometry. In addition, DDX5 knockdown inhibited the MG63 cell migration and invasion on transwell assays. Further experiments showed that DDX5 knockdown not only inhibited the expression of TCF12 but also decreased the mRNA and protein levels of Cyclin E1, an important regulator of G1-S phase progression, suggesting that DDX5 was required for the entry of cells into S phase. Overexpression of TCF12 reversed the cell proliferation, migration and invasion in MG63 cells induced by DDX5 knockdown accompanied by the upregulation of Cyclin E1. Additionally, we observed that DDX5 interacted with TCF12 in both OS tissues and MG63 cells by Co-immunoprecipitation assays. Taken together, our study revealed that DDX5 interacts with TCF12 and promotes the progression of OS by stimulating cell cycle progression. Our results suggest that DDX5 and TCF12 could be potential biomarkers for the diagnosis and treatment of OS.
Insights
DEAD-box helicase 5 (DDX5) and transcription factor 12 (TCF12) are overexpressed in osteosarcoma (OS). DDX5 interacts with TCF12, promoting OS progression and poor prognosis, suggesting potential diagnostic and therapeutic roles.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Osteosarcoma (OS) is a primary bone cancer with poorly understood development mechanisms and limited effective treatments.
- The DEAD-box helicase 5 (DDX5) protein is implicated in various oncogenic processes.
- Transcription factor 12 (TCF12) is a key molecule in the Wnt signaling pathway, relevant to cancer progression.
Purpose of the Study:
- To investigate the role of DDX5 in osteosarcoma (OS) development and progression.
- To explore the relationship between DDX5 and transcription factor 12 (TCF12) in OS.
- To assess the potential of DDX5 and TCF12 as biomarkers for OS diagnosis and treatment.
Main Methods:
- Expression analysis of DDX5 and TCF12 in OS tissues and cell lines (MG63) versus normal tissues and osteoblast cells (hFOB 1.19).
- In vitro assays including MTS, EdU proliferation, flow cytometry for apoptosis, and transwell assays for migration and invasion.
- Co-immunoprecipitation assays to confirm protein-protein interaction between DDX5 and TCF12.
Main Results:
- DDX5 and TCF12 protein levels were significantly elevated in OS tissues and MG63 cells.
- High expression of DDX5 and TCF12 correlated with adverse clinicopathological features and poor prognosis in OS patients.
- DDX5 knockdown inhibited cell proliferation, migration, and invasion, while promoting apoptosis in MG63 cells, and reduced Cyclin E1 expression.
- TCF12 overexpression counteracted the effects of DDX5 knockdown on cell proliferation, migration, and invasion.
- DDX5 was found to interact with TCF12 in OS cells and tissues.
Conclusions:
- DDX5 interacts with TCF12 and promotes osteosarcoma progression by enhancing cell cycle progression.
- The DDX5-TCF12 axis plays a critical role in OS development and aggressiveness.
- DDX5 and TCF12 represent promising biomarkers for osteosarcoma diagnosis and therapeutic targeting.
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