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Updated: Mar 9, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
HELQ reverses the malignant phenotype of osteosarcoma cells via CHK1-RAD51 signaling pathway
Dong Ning Liu1, Yun Fei Zhou2, Ai Fen Peng3
1Southern Medical University, Guangzhou, Guangdong, P.R. China.
Abstract:
HELQ is a DNA helicase important for repair of DNA lesions and has been linked to several types of cancer. However, little is known about its relationship with osteosarcoma (OS) and its mechanism. In the present study, the expression of HELQ and its downstream mediators in OS cells was assayed by quantitative PCR and western blot analysis. The function of HELQ in OS cells was investigated by Transwell invasion, wound healing, CCK8 assays and Comet assay. The results demonstrated that HELQ gene and protein were expressed in OS cells. OS cell invasion, migration, proliferation and DNA damage repair were enhanced by HELQ knock-down with shRNA-lentivirus and inhibited by HELQ overexpression with lentivirus transfection. Furthermore, the antitumor activities of HELQ may be associated with upregulated expression of the DNA damage-related proteins CHK1 and RAD51. Our findings indicated that HELQ confers an anti-invasive phenotype on OS cells by activating the CHK1-RAD51 signaling pathway and suggested that HELQ could be recognized as a promising therapeutic target for OS and other types of malignant tumors.
Insights
The DNA helicase HELQ promotes osteosarcoma cell invasion, migration, and DNA repair. Inhibiting HELQ may offer a new therapeutic strategy for osteosarcoma (OS) and other cancers.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- HELQ is a DNA helicase crucial for DNA lesion repair and implicated in various cancers.
- The specific role and mechanism of HELQ in osteosarcoma (OS) remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression and function of HELQ in osteosarcoma cells.
- To elucidate the mechanism by which HELQ influences OS progression and DNA repair.
Main Methods:
- Quantitative PCR and Western blot analysis for gene and protein expression.
- Functional assays including Transwell invasion, wound healing, CCK8, and Comet assays.
- Genetic manipulation using shRNA-lentivirus for knock-down and lentivirus transfection for overexpression.
Main Results:
- HELQ gene and protein are expressed in OS cells.
- HELQ knockdown enhanced OS cell invasion, migration, proliferation, and DNA damage repair.
- HELQ overexpression inhibited these processes.
- Antitumor effects of HELQ are linked to upregulated CHK1 and RAD51 expression.
Conclusions:
- HELQ promotes an invasive phenotype in OS cells via the CHK1-RAD51 signaling pathway.
- HELQ represents a potential therapeutic target for osteosarcoma and other malignancies.
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