Detailed Information on Publication Record
2016
The dual role of asporin in breast cancer progression
SIMKOVA, D., G. KHARAISHVILI, G. KORINKOVA, T. OZDIAN, T. SUCHANKOVA-KLEPLOVA et. al.Basic information
Original name
The dual role of asporin in breast cancer progression
Authors
SIMKOVA, D. (203 Czech Republic), G. KHARAISHVILI (268 Georgia), G. KORINKOVA (203 Czech Republic), T. OZDIAN (203 Czech Republic), T. SUCHANKOVA-KLEPLOVA (203 Czech Republic), T. SOUKUP (203 Czech Republic), M. KRUPKA (203 Czech Republic), A. GALANDAKOVA (203 Czech Republic), P. DZUBAK (203 Czech Republic), M. JANIKOVA (203 Czech Republic), J. NAVRATIL (203 Czech Republic), Z. KAHOUNOVA (203 Czech Republic), Karel SOUČEK (203 Czech Republic, belonging to the institution) and J. BOUCHAL (203 Czech Republic, guarantor)
Edition
Oncotarget, Albany, Impact Journals, 2016, 1949-2553
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
10601 Cell biology
Country of publisher
United States of America
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 5.168
RIV identification code
RIV/00216224:14310/16:00100455
Organization unit
Faculty of Science
UT WoS
000385429100101
Keywords in English
asporin; 3D cultivation; stiffness; grade; breast cancer
Tags
International impact, Reviewed
Změněno: 22/3/2018 10:15, Mgr. Radek Ševčík, Ph.D.
Abstract
V originále
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.