|Awarded On||February 18, 2015|
|Title||Understanding How NCOA6 Suppresses Endometrial Cancer by Inhibiting the Wnt/beta-Catenin Pathway|
|Award Mechanism||Individual Investigator|
|Institution/Organization||Baylor College of Medicine|
|Principal Investigator/Program Director||Jianming Xu|
|Cancer Sites||Cervix Uteri|
Endometrial cancer (EMC) is a disease with high mortality. Enhanced uterine (U) sensitivity to estrogen (E), activation of the Wnt/beta-catenin (W/bC) pathway and inactivation of the Pten tumor suppressor are main driving forces of EMC. However, it is unknown what controls the U E sensitivity and holds the W/bC activity to prevent EMC. Our preliminary study suggests that NCOA6, a gene expression coregulator, may be a potent suppressor of EMC by inhibiting the U E sensitivity and W/bC activation. We found NCOA6 is frequently mutated in human EMC. Deletion of NCOA6 from mouse uterus increased E sensitivity, activated the W/bC pathway, caused EMC development and accelerated the growth of EMC wi...