Metadherin regulates radioresistance in cervical cancer cells

Zhao,Ying; Moran,Meena  S.; Yang,Qifeng; Liu,Qiao; Yuan,Cunzhong; Hong,Shuhui; Kong,Beihua

doi:10.3892/or.2012.1692

Metadherin regulates radioresistance in cervical cancer cells

Authors:
- Ying Zhao
- Meena S. Moran
- Qifeng Yang
- Qiao Liu
- Cunzhong Yuan
- Shuhui Hong
- Beihua Kong
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Affiliations: Department of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Ji'nan, Shandong 250012, P.R. China, Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT, USA, Department of Breast Surgery, Qilu Hospital of Shandong University, Ji'nan, Shandong 250012, P.R. China, Institute of Molecular Medicine and Genetics and Key Laboratory of Experimental Teratology, Ministry of Education, Shandong University School of Medicine, Ji'nan, Shandong 250012, P.R. China, Department of Obstetrics and Gynecology, Affiliated Qianfoshan Hospital of Shandong University, Ji'nan, Shandong 250014, P.R. China
Published online on: February 20, 2012 https://doi.org/10.3892/or.2012.1692
Pages: 1520-1526

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Abstract

Metadherin (MTDH) promotes cancer metastasis, chemoresistance, invasion and angiogenesis. Upregulation of MTDH is correlated with both progression and poor clinical outcome of many types of cancers; however, there is currently no information regarding the role of MTDH in radiation sensitivity. Here, we investigated the effects of MTDH on the radiosensitivity of cervical cancer cells using the SiHa cell line. We discovered that cervical cancer cells in which MTDH was knocked down had significantly increased radiosensitivity as measured by a clonogenic assay. MTDH knockdown cells also had increased apoptosis and a decreased proportion of cells arrested in the G2 phase after radiation treatment. MTDH knockdown also weakened the repair of DNA double-strand breaks (DSBs) induced by radiation. These results indicate that MTDH affects the radiosensitivity of cervical cancer cells and that MTDH may be a novel target to improve cervical cancer radiation response.