• Open Access

Overexpression of DNA polymerase iota (Polι) in esophageal squamous cell carcinoma

Authors

  • Jundong Zhou,

    1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, China
    2. Department of Radio-Oncology, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, China
    3. Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
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    • These authors contributed equally to this study.
  • Shuyu Zhang,

    1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, China
    2. Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
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    • These authors contributed equally to this study.
  • Ling Xie,

    1. Department of Radio-Oncology, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, China
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    • These authors contributed equally to this study.
  • Pengfei Liu,

    1. Department of Gastroenterology, The Affiliated Jiangyin Hospital of Southeast University, Jiangyin, China
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  • Fang Xie,

    1. The State Key Laboratory of Genetic Engineering and School of Life Science, Fudan University, Shanghai, China
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  • Jinchang Wu,

    Corresponding author
    1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, China
    2. Department of Radio-Oncology, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, China
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  • Jianping Cao,

    Corresponding author
    1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, China
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  • Wei-Qun Ding

    1. Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA
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Abstract

The present study investigated the transcriptional regulation of low-fidelity translesion DNA synthesis (TLS) polymerases in human esophageal carcinoma. Significantly higher mRNA expression of polymerase zeta (Polξ), RAD18, polymerase iota (Polι), and polymerase kappa (Polκ) was found in esophageal carcinomas. The increased expression of Polι in tumor samples was further confirmed by immunohistochemistry. The promoter of POLI that encodes Polι was found to be hypomethylated, although the overexpression of this gene was unlikely to be associated with methylation in tumors. We further identified Sp1 and Oct-1 binding sites present in the POLI promoter. We observed that the binding affinity of Sp1 to the POLI promoter was significantly increased in cancerous tissues and that Sp1 activated POLI gene transcription in cultured cell lines. The present study demonstrates overexpression of the TLS genes in esophageal carcinoma and identifies a key role for Sp1 in upregulating POLI gene expression. (Cancer Sci, doi: 10.1111/j.1349-7006.2012.02309.x, 2012)

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