Abstract
Female Eker rats harboring an insertional deletion in one copy of the tuberous sclerosis complex 2 (Tsc2) gene develop uterine leiomyoma, but the underlying mechanism of human uterine leiomyoma is not completely understood. To examine whether down-regulation of tuberin, a TSC2 gene product, is present in human uterine leiomyoma, we analyzed leiomyoma and matched myometrium tissues from 22 Chinese patients with Western blotting and real-time polymerase chain reaction analyses, and found that the expression of tuberin was significantly increased in leiomyoma tissues compared with matched myometrium tissues with inhibition of both the mammalian target of rapacmycin pathway and mitogen-activated protein kinase pathways.
Copyright © 2011 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adult
-
Case-Control Studies
-
Female
-
Gene Expression Regulation, Neoplastic
-
Humans
-
Leiomyoma / genetics*
-
Leiomyoma / metabolism
-
Leiomyoma / pathology
-
Middle Aged
-
Mitogen-Activated Protein Kinase 1 / metabolism
-
Mitogen-Activated Protein Kinase 3 / metabolism
-
Myometrium / metabolism*
-
Myometrium / pathology
-
TOR Serine-Threonine Kinases / genetics
-
TOR Serine-Threonine Kinases / metabolism
-
Tuberous Sclerosis Complex 2 Protein
-
Tumor Suppressor Proteins / genetics*
-
Tumor Suppressor Proteins / metabolism
-
Up-Regulation
-
Uterine Neoplasms / genetics*
-
Uterine Neoplasms / metabolism
-
Uterine Neoplasms / pathology
Substances
-
TSC2 protein, human
-
Tsc2 protein, rat
-
Tuberous Sclerosis Complex 2 Protein
-
Tumor Suppressor Proteins
-
MTOR protein, human
-
TOR Serine-Threonine Kinases
-
Mitogen-Activated Protein Kinase 1
-
Mitogen-Activated Protein Kinase 3