LMP2/b1i as a potential biomarker of human uterine mesenchymal tumors under the combination of candidate molecules, cyclin E and calponin h1

Abstract

Takuma Hayashi

Uterine leiomyosarcoma (Ut-LMS) develops more frequently in the myometrium of the uterine body than in the uterine cervix. Although, the development of gynecological tumors is often correlated with the secretion of female hormones that of Ut-LMS does not, and its risk factor(s) remain unknown. Importantly, a diagnostic biomarker that can distinguish malignant tumor Ut-LMS from benign tumor leiomyoma (LMA) has yet to be established. Therefore, the risk factor(s) associated with Ut-LMS need to be examined in order to establish a diagnosis and clinical treatment method. Mice with a homozygous deficiency for the proteasome β-ring subunit, low-molecular mass polypeptide (LMP) 2/β1i spontaneously develop Ut-LMS, with a disease prevalence of ~40% by 14 months of age. In a recent study, we showed that LMP2/β1i expression was absent in human Ut-LMS, but present in other human uterine mesenchymal tumors including uterine LMA. Moreover, LMP2/β1i is also known to negatively regulate human Ut-LMS tumorigenesis. Additional experiments furthermore revealed the differential expression of cyclin E and calponin h1 in human uterine mesenchymal tumors. Therefore, LMP2/ β1i is a potential diagnostic biomarker when combined with the candidate molecules, cyclin E and calponin h1 for human Ut-LMS, and may be a targeted molecule for a new therapeutic approach.