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Biological Significance of the Proteasome Subunit LMP2/b1i as a Tumor Suppressor in Human Uterine Leiomyosarcoma

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Zeitschriftentitel: Journal of Cancer Research Updates
Personen und Körperschaften: Takuma Hayashi, Akiko Horiuchi, Kenji Sano, Gal Gur, Hiroyuki Aburatani, Osamu Ishiko, Nobuo Yaegashi, Tanri Shiozawa, Yae Kanai, Dorit Zharhary, Susumu Tonegawa, Ikuo Konishi
In: Journal of Cancer Research Updates, 1, 2012, 2, S. 181-188
Format: E-Article
Sprache: Unbestimmt
veröffentlicht:
Neoplasia Research
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Zusammenfassung: <jats:p> Uterine leiomyosarcoma (Ut-LMS) develops more often in the muscle tissue layer of the uterine body than in the uterine cervix. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of Ut-LMS is not substantially correlated with hormonal conditions, and the risk factors are not yet known. Importantly, a diagnostic-biomarker which distinguishes malignant Ut-LMS from other uterine mesenchymal tumors including leiomyoma (LMA) is yet to be established. Accordingly, it is necessary to analyze risk factors associated with Ut-LMS, to establish a clinical treatment method. Proteasome subunit, low-molecular mass polypeptide(LMP2)/b1i-deficient mice spontaneously develop Ut-LMS, with a disease prevalence of ~40% by 14 months of age. Recent experiments with human and mouse uterine tissues revealed defective LMP2/b1i expression in human Ut-LMS that was traced to the interferon (IFN)-g pathway and a specific effect of Janus kinase (JAK)-1 somatic mutations on LMP2/b1i transcriptional activation. Furthermore, analysis of a human Ut-LMS cell line clarified the biological significance of LMP2/b1i in malignant myometrium transformation and the cell cycle, thus implicating LMP2/b1i as an anti-tumorigenic candidate. Therefore, defective-LMP2/b1i expression may be a risk factor for human Ut-LMS. LMP2/b1i is a potential diagnostic-biomarker for Ut-LMS, and may be a targeted-molecule for a new clinical therapeutic approach. </jats:p>
Umfang: 181-188
ISSN: 1929-2279
DOI: 10.6000/1929-2279.2012.01.02.4