Differential miRNA expression defines migration and reduced apoptosis in follicular thyroid carcinomas

详细信息    查看全文

• 作者：Bartosz Wojtas^a ; ¹ ; ^{bwojtas@io.gliwice.pl" class="auth_mail} ; Carolina Ferraz^b ; ¹ ; ^{carolina.ferraz.endocrinologia@gmail.com" class="auth_mail} ; Tomasz Stokowy^a ; ^c ; ^{tomasz.stokowy@polsl.pl" class="auth_mail} ; Steffen Hauptmann^d ; ^{steffen.hauptmann@gmx.de" class="auth_mail} ; Dariusz Lange^e ; ^{dlange@io.gliwice.pl" class="auth_mail} ; Henning Dralle^f ; ^{henning.dralle@medizin.uni-halle.de" class="auth_mail} ; Thomas Musholt^g ; ^{musholt@uni-mainz.de" class="auth_mail} ; Barbara Jarzab^a ; ^{bjarzab@io.gliwice.pl" class="auth_mail} ; Ralf Paschke^b ; ^{Ralf.Paschke@medizin.uni-leipzig.de" class="auth_mail} ; Markus Eszlinger^b ; ^{Markus.Eszlinger@medizin.uni-leipzig.de" class="auth_mail}
• 关键词：miRNA ; Migration ; Apoptosis ; Follicular thyroid cancer
• 刊名：Molecular and Cellular Endocrinology
• 出版年：5 May, 2014
• 年：2014
• 卷：388
• 期：1-2
• 页码：1-9
• 全文大小：1014 K

文摘

The objective of the study was to identify microRNAs (miRs) characteristic for follicular thyroid carcinoma (FTC) and to define their role in tumorigenesis. A miR-microarray study was conducted to identify miRs differentially expressed between FTCs and their surrounding tissues. Selection was further reinforced by a literature review. Four miRs were selected and confirmed by RT-qPCR: miR-146b, -183, -221 were up-regulated, whereas miR-199b down-regulated in FTCs. The influence of these miRs on cell proliferation, cell cycle, apoptosis and migration was studied in HTori and FTC-133 cells. Functional characterization suggests an impact of miR-183 and miR-146b in FTC development. Overexpression of both miRs significantly induces migration. Moreover, overexpression of miR-183 significantly represses apoptosis. MiR-199b and -221 do not have significant effects on proliferation, cell cycle, apoptosis or migration in HTori and FTC-133 cells. Our data suggest that miR-146b and miR-183 may influence FTC development through the induction of migration and apoptosis inhibition.