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APOBEC3B Does Not Promote Tumor Progression in Tp53 Hemizygous Mice
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  • Yoshihito Horisawa,
  • Tadahiko Matsumoto,
  • June Takeda,
  • Yusuke Tashiro,
  • Ryosuke Nomura,
  • Suguru Takeuchi,
  • Yugo Kawai,
  • Yasuhiro Kazuma,
  • Yoshinobu Konishi,
  • Hiroyuki Yamazaki,
  • Hiroyuki Matsui,
  • Kotaro Shirakawa,
  • Akifumi Takaori-Kondo
Yoshihito Horisawa
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Tadahiko Matsumoto
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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June Takeda
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Yusuke Tashiro
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Ryosuke Nomura
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Suguru Takeuchi
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Yugo Kawai
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Yasuhiro Kazuma
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Yoshinobu Konishi
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Hiroyuki Yamazaki
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Hiroyuki Matsui
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Kotaro Shirakawa
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku

Corresponding Author:[email protected]

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Akifumi Takaori-Kondo
Kyoto Daigaku Daigakuin Igaku Kenkyuka Igakubu Ketsueki Naikagaku
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Abstract

DNA cytosine deaminase APOBEC3B (A3B) is one of the endogenous sources of somatic mutations in many types of human cancers and is associated with tumor progression rather than tumorigenesis. However, it remains uncertain whether APOBEC3B-induced mutations accelerate tumor progression or not. In this paper, we established a mouse model with A3B overexpression and investigated whether the introduction of A3B overexpression accelerates tumor development in Tp53 hemizygous mice. A3B expression was validated by qPCR, immunoblotting, and immunohistochemistry in mouse tissues, and in vitro CDA assays revealed that A3B has its CDA activity in mouse tissues. However, we did not observe any difference in tumor development between the mice with or without A3B expression. A3B expression and its CDA activity were confirmed in tumor tissues of mice overexpressing A3B. Therefore, we concluded that the introduction of A3B overexpression did not accelerate tumor development in Tp53 hemizygous mice. Our mouse model with A3B overexpression is well-validated and useful for further research.