Conditional abrogation of transforming growth factor-β receptor 1 in PTEN-inactivated endometrium promotes endometrial cancer progression in mice.

ABSTRACT: Although a putative role for transforming growth factor-β (TGFB) signalling in the pathogenesis of human endometrial cancer has long been proposed, the precise function of TGFB signalling in the development and progression of endometrial cancer remains elusive. Depletion of phosphatase and tensin homologue (PTEN) in the mouse uterus causes endometrial cancer. To identify the potential role of TGFB signalling in endometrial cancer, we simultaneously deleted TGFB receptor 1 (Tgfbr1) and Pten in the mouse uterus by using Cre-recombinase driven by the progesterone receptor (termed Pten^d/d ;Tgfbr1^d/d ). We found that Pten^d/d ;Tgfbr1^d/d mice developed severe endometrial lesions that progressed more rapidly than those resulting from conditional deletion

SUBMITTER: Gao Y 

PROVIDER: S-EPMC5568928 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature