AI Article Synopsis
- Zinc finger X-chromosomal protein (ZFX) is implicated in various cancers, but its role in osteosarcoma was previously unexplored.
- Research showed that knocking down ZFX in osteosarcoma cells reduced their ability to grow and form colonies, indicating ZFX promotes cancer cell proliferation.
- The study found that ZFX knockdown caused cell cycle arrest and increased cell death, suggesting that targeting ZFX could be a potential strategy for treating osteosarcoma.
Article Abstract
Zinc finger X-chromosomal protein (ZFX) is a member of the zinc finger family of proteins. The importance of ZFX in several cancer types, including prostate cancer, laryngeal squamous cell carcinoma, and glioma, has been addressed. However, the role of ZFX in human osteosarcoma remains unknown. Here we investigated the phenotype of ZFX knockdown on cell proliferation and in vitro tumorigenesis using lentivirus-mediated loss-of-function strategy. The results demonstrated that the proliferation and colony formation ability of human osteosarcoma Saos-2 and MG63 cells was impaired by ZFX small interfering RNA (siRNA)-expressing lentivirus. Moreover, loss of ZFX led to G0/G1 phase cell cycle arrest and a significant increase of cells in the sub-G1 fraction, indicating that ZFX functions as an oncogene in the malignant proliferation process in osteosarcoma. Furthermore, ZFX siRNA may have an antitumorigenic effect on osteosarcoma cells. Our findings hold important significance for RNA interference-mediated cancer gene therapy for human osteosarcoma.
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| http://dx.doi.org/10.3727/096504013X13775486749290 | DOI Listing |
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