Premium
microRNA‐Mediated Survivin Control of Pluripotency
Author(s) -
Kapinas Kristina,
Kim Heesun,
Mandeville Matthew,
MartinBuley Lori A.,
Croce Carlo M.,
Lian Jane B.,
van Wijnen Andre J.,
Stein Janet L.,
Altieri Dario C.,
Stein Gary S.
Publication year - 2015
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24681
Subject(s) - survivin , homeobox protein nanog , nanog homeobox protein , embryonic stem cell , biology , microrna , microbiology and biotechnology , gene isoform , cancer cell , transcription factor , sox2 , cancer research , induced pluripotent stem cell , cancer , genetics , gene
Understanding the mechanisms that sustain pluripotency in human embryonic stem cells (hESCs) is an active area of research that may prove useful in regenerative medicine and will provide fundamental information relevant to development and cancer. hESCs and cancer cells share the unique ability to proliferate indefinitely and rapidly. Because the protein survivin is uniquely overexpressed in virtually all human cancers and in hESCs, we sought to investigate its role in supporting the distinctive capabilities of these cell types. Results presented here suggest that survivin contributes to the maintenance of pluripotency and that post‐transcriptional control of survivin isoform expression is selectively regulated by microRNAs. miR‐203 has been extensively studied in human tumors, but has not been characterized in hESCs. We show that miR‐203 expression and activity is consistent with the expression and subcellular localization of survivin isoforms that in turn modulate expression of the Oct4 and Nanog transcription factors to sustain pluripotency. This study contributes to understanding of the complex regulatory mechanisms that govern whether hESCs proliferate or commit to lineages. J. Cell. Physiol. 230: 63–70, 2015. © 2014 Wiley Periodicals, Inc.