The knockdown of H19lncRNA reveals its regulatory role in pluripotency and tumorigenesis of human embryonic carcinoma cells

Evelyne Zeira, Rinat Abramovitch, Karen Meir, Sharona Even Ram, Yaniv Gil, Baruch Bulvik, Zohar Bromberg, Or Levkovitch, Nathalie Nahmansson, Revital Adar, Benjamin Reubinoff, Eithan Galun, Michal Gropp*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

The function of imprinted H19 long non-coding RNA is still controversial. It is highly expressed in early embryogenesis and decreases after birth and re-expressed in cancer. To study the role of H19 in oncogenesis and pluripotency, we down-regulated H19 expression in vitro and in vivo in pluripotent human embryonic carcinoma (hEC) and embryonic stem (hES) cells. H19 knockdown resulted in a decrease in the expression of the pluripotency markers Oct4, Nanog, TRA-1-60 and TRA-1-81, and in the up-regulation of SSEA1; it further attenuated cell proliferation, decreased cell-matrix attachment, and up-regulated E-Cadherin expression. SCID-Beige mice transplanted with H19 down-regulated hEC cells exhibited slower kinetics of tumor formation, resulting in an increased animal survival. Tumors derived from H19 down-regulated cells showed a decrease in the expression of pluripotency markers and up-regulation of SSEA-1 and E-cadherin. Our results suggest that H19 oncogenicity in hEC cells is mediated through the regulation of the pluripotency state.

Original languageAmerican English
Pages (from-to)34691-34703
Number of pages13
JournalOncotarget
Volume6
Issue number33
DOIs
StatePublished - 2015
Externally publishedYes

Keywords

  • H19lncRNA
  • HEC cells
  • Oncogenesis
  • Pluripotency

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