| Literature DB >> 22659265 |
Takuma Hayashi1, Akiko Horiuchi, Kenji Sano, Nobuyoshi Hiraoka, Mari Kasai, Tomoyuki Ichimura, Tamotsu Sudo, Ryuichiro Nishimura, Osamu Ishiko, Tanri Shiozawa, Yae Kanai, Nobuo Yaegashi, Hiroyuki Aburatani, Ikuo Konishi.
Abstract
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.Entities:
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Year: 2012 PMID: 22659265 DOI: 10.1016/j.febslet.2012.05.029
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124