Department of Immunology and Infectious Disease, Shinshu University Graduate School of Medicine, Nagano 390-8621, Japan.
FEBS Lett. 2012 Jun 21;586(13):1824-31. doi: 10.1016/j.febslet.2012.05.029. Epub 2012 May 29.
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.
子宫平滑肌肉瘤（LMS）是一种高度转移性的平滑肌肿瘤，钙调蛋白 h1 被怀疑具有肿瘤抑制因子的生物学作用。我们之前的研究报告表明，LMP2 缺失的小鼠通过子宫肌层的恶性转化自发发展为子宫 LMS，这表明该蛋白也是一种抗肿瘤候选物。在本研究中，我们表明 LMP2 可能独立于其在蛋白酶体中的作用负调节 LMS。此外，有几项证据表明，尽管钙调蛋白 h1 不会直接影响肿瘤发生，但它显然会影响 LMP2 诱导的细胞形态变化。LMP2 的调节可能会为人类子宫 LMS 带来新的治疗方法。
