Speckle‑type POZ (pox virus and zinc finger protein) protein gene deletion in ovarian cancer: Fluorescence in situ hybridization analysis of a tissue microarray

Hu,Xiaoyu; Yang,Zhu; Zeng,Manman; Liu,Yi; Yang,Xiaotao; Li,Yanan; Li,Xu; Yu,Qiubo

doi:10.3892/ol.2016.4643

Speckle‑type POZ (pox virus and zinc finger protein) protein gene deletion in ovarian cancer: Fluorescence in situ hybridization analysis of a tissue microarray

Authors:
- Xiaoyu Hu
- Zhu Yang
- Manman Zeng
- Yi Liu
- Xiaotao Yang
- Yanan Li
- Xu Li
- Qiubo Yu
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Affiliations: Department of Gynecology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P.R. China, Molecular Medical Laboratory, Chongqing Medical University, Chongqing 400016, P.R. China
Published online on: May 30, 2016 https://doi.org/10.3892/ol.2016.4643
Pages: 658-662

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Abstract

The aim of the present study was to investigate the status of speckle‑type POZ (pox virus and zinc finger protein) protein (SPOP) gene located on chromosome 17q21 in ovarian cancer (OC). The present study evaluated a tissue microarray, which contained 90 samples of ovarian cancer and 10 samples of normal ovarian tissue, using fluorescence in situ hybridization (FISH). FISH is a method where a SPOP‑specific DNA red fluorescence probe was used for the experimental group and a centromere‑specific DNA green fluorescence probe for chromosome 17 was used for the control group. The present study demonstrated that a deletion of the SPOP gene was observed in 52.27% (46/88) of the ovarian cancer tissues, but was not identified in normal ovarian tissues. Simultaneously, monosomy 17 was frequently identified in the ovarian cancer tissues, but not in the normal ovarian tissues. Furthermore, the present data revealed that the ovarian cancer histological subtype and grade were significantly associated with a deletion of the SPOP gene, which was assessed by the appearance of monosomy 17 in the ovarian cancer samples; the deletion of the SPOP gene was observed in a large proportion of serous epithelial ovarian cancer (41/61; 67.21%), particularly in grade 3 (31/37; 83.78%). In conclusion, deletion of the SPOP gene on chromosome 17 in ovarian cancer samples, which results from monosomy 17, indicates that the SPOP gene may serve as a tumor suppressor gene in ovarian cancer.

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