کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2048231 | 1074071 | 2012 | 8 صفحه PDF | دانلود رایگان |

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.
► Uterine leiomyosarcoma (LMS) is highly metastatic smooth muscle neoplasm.
► LMP2 negatively regulates uterine LMS independently of its role in the proteasome.
► Calponin h1 clearly affects LMP2-induced cellular morphological changes.
► The role of LMP2 as tumor suppressor leads to new therapeutic targets in uterine LMS.
Journal: FEBS Letters - Volume 586, Issue 13, 21 June 2012, Pages 1824–1831