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抄録

Uterine leiomyosarcoma (LMS) is a highly metastatic smooth muscle neoplasm for which calponin h1 is suspected to have a biological role as a tumor-suppressor. We earlier reported that LMP2-null mice spontaneously develop uterine LMS through malignant transformation of the myometrium, thus implicating this protein as an anti-tumorigenic candidate as well. In the present study, we show that LMP2 may negatively regulate LMS independently of its role in the proteasome. Moreover, several lines of evidence indicate that although calponin h1 does not directly influence tumorigenesis, it clearly affects LMP2-induced cellular morphological changes. Modulation of LMP2 may lead to new therapeutic approaches in human uterine LMS.

収録刊行物

  • FEBS LETTERS

    FEBS LETTERS 586(13), 1824-1831, 2012-06-21

    ELSEVIER SCIENCE BV

各種コード

  • NII論文ID(NAID)
    120005440157
  • NII書誌ID(NCID)
    AA00642943
  • 本文言語コード
    ENG
  • 資料種別
    journal article
  • データ提供元
    IR 
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