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.

Oncology Reports
|December 22, 2016
PubMed

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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