2016
Simkova, Dana; Kharaishvili, Gvantsa; Korinkova, Gabriela; Ozdian, Tomas; Suchánková-Kleplová, Tereza; Soukup, Tomas; Krupka, Michal; Galandakova, Adela; Dzubak, Petr; Janikova, Maria; Navratil, Jiri; Kahounova, Zuzana; Soucek, Karel; Bouchal, Jan
The dual role of asporin in breast cancer progression. Journal Article
In: Oncotarget, vol. 7, no. 32, pp. 52045–52060, 2016, ISSN: 1949-2553, (Place: United States).
Abstract | Links | BibTeX | Tags: 3D cultivation, asporin, Breast cancer, Breast Neoplasms/metabolism/mortality/*pathology, Disease-Free Survival, Extracellular Matrix Proteins/*metabolism, Female, Fibroblasts/metabolism/pathology, grade, Humans, Kaplan-Meier Estimate, Prognosis, stiffness, Tumor Microenvironment/physiology
@article{simkova_dual_2016,
title = {The dual role of asporin in breast cancer progression.},
author = {Dana Simkova and Gvantsa Kharaishvili and Gabriela Korinkova and Tomas Ozdian and Tereza Suchánková-Kleplová and Tomas Soukup and Michal Krupka and Adela Galandakova and Petr Dzubak and Maria Janikova and Jiri Navratil and Zuzana Kahounova and Karel Soucek and Jan Bouchal},
doi = {10.18632/oncotarget.10471},
issn = {1949-2553},
year = {2016},
date = {2016-08-01},
journal = {Oncotarget},
volume = {7},
number = {32},
pages = {52045–52060},
abstract = {Asporin has been reported as a tumor suppressor in breast cancer, while asporin-activated invasion has been described in gastric cancer. According to our in silico search, high asporin expresion associates with significantly better relapse free survival (RFS) in patients with low-grade tumors but RFS is significantly worse in patients with grade 3 tumors. In line with other studies, we have confirmed asporin expression by RNA scope in situ hybridization in cancer associated fibroblasts. We have also found asporin expression in the Hs578T breast cancer cell line which we confirmed by quantitative RT-PCR and western blotting. From multiple testing, we found that asporin can be downregulated by bone morphogenetic protein 4 while upregulation may be facilited by serum-free cultivation or by three dimensional growth in stiff Alvetex scaffold. Downregulation by shRNA inhibited invasion of Hs578T as well as of CAFs and T47D cells. Invasion of asporin-negative MDA-MB-231 and BT549 breast cancer cells through collagen type I was enhanced by recombinant asporin. Besides other investigations, large scale analysis of aspartic acid repeat polymorphism will be needed for clarification of the asporin dual role in progression of breast cancer.},
note = {Place: United States},
keywords = {3D cultivation, asporin, Breast cancer, Breast Neoplasms/metabolism/mortality/*pathology, Disease-Free Survival, Extracellular Matrix Proteins/*metabolism, Female, Fibroblasts/metabolism/pathology, grade, Humans, Kaplan-Meier Estimate, Prognosis, stiffness, Tumor Microenvironment/physiology},
pubstate = {published},
tppubtype = {article}
}
Asporin has been reported as a tumor suppressor in breast cancer, while asporin-activated invasion has been described in gastric cancer. According to our in silico search, high asporin expresion associates with significantly better relapse free survival (RFS) in patients with low-grade tumors but RFS is significantly worse in patients with grade 3 tumors. In line with other studies, we have confirmed asporin expression by RNA scope in situ hybridization in cancer associated fibroblasts. We have also found asporin expression in the Hs578T breast cancer cell line which we confirmed by quantitative RT-PCR and western blotting. From multiple testing, we found that asporin can be downregulated by bone morphogenetic protein 4 while upregulation may be facilited by serum-free cultivation or by three dimensional growth in stiff Alvetex scaffold. Downregulation by shRNA inhibited invasion of Hs578T as well as of CAFs and T47D cells. Invasion of asporin-negative MDA-MB-231 and BT549 breast cancer cells through collagen type I was enhanced by recombinant asporin. Besides other investigations, large scale analysis of aspartic acid repeat polymorphism will be needed for clarification of the asporin dual role in progression of breast cancer.