Table of Contents Author Guidelines Submit a Manuscript
Disease Markers
Volume 2017, Article ID 8248175, 14 pages
https://doi.org/10.1155/2017/8248175
Research Article

Type II Endometrial Cancer Overexpresses NILCO: A Preliminary Evaluation

1Department of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, GA, USA
2Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA, USA
3Department of Obstetrics and Gynecology, Morehouse School of Medicine, Atlanta, GA, USA
4Department of Community Health & Preventive Medicine, Morehouse School of Medicine, Atlanta, GA, USA

Correspondence should be addressed to Ruben Rene Gonzalez-Perez; ude.msm@zelaznogr

Received 12 January 2017; Accepted 27 April 2017; Published 4 June 2017

Academic Editor: Eric A. Singer

Copyright © 2017 Danielle Daley-Brown et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. The expression of NILCO molecules (Notch, IL-1, and leptin crosstalk outcome) and the association with obesity were investigated in types I and II endometrial cancer (EmCa). Additionally, the involvement of NILCO in leptin-induced invasiveness of EmCa cells was investigated. Methods. The expression of NILCO mRNAs and proteins were analyzed in EmCa from African-American and Chinese patients (tissue array, cases). The role of NILCO in leptin-induced invasion of Ishikawa and An3ca EmCa cells was investigated using Notch, IL-1, and leptin signaling inhibitors. Results. NILCO molecules were expressed higher in type II EmCa, regardless of ethnic background or obesity status of patients. NILCO proteins were mainly localized in the cellular membrane and cytoplasm of type II EmCa. Additionally, EmCa from obese African-American patients showed higher levels of NILCO molecules than EmCa from lean patients. Notably, leptin-induced EmCa cell invasion was abrogated by NILCO inhibitors. Conclusion. Type II EmCa expressed higher NILCO molecules, which may suggest it is involved in the progression of the more aggressive EmCa phenotype. Obesity was associated with higher expression of NILCO molecules in EmCa. Leptin-induced cell invasion was dependent on NILCO. Hence, NILCO might be involved in tumor progression and could represent a new target/biomarker for type II EmCa.