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Recent evidence indicates that long noncoding RNAs (lncRNAs) have a critical role in the regulation of cellular processes such as differentiation, proliferation, and metastasis. These lncRNAs are dysregulated in a variety of cancers and many function as tumor suppressors; however, the regulatory factors involved in silencing lncRNA transcription are poorly understood. In this study, we showed that epigenetic silencing of lncRNA SPRY4 intronic transcript 1 ( SPRY4-IT1 ) occurs in non-small-cell lung cancer (NSCLC) cells through direct transcriptional repression mediated by the Polycomb group protein enhancer of zeste homolog 2 (EZH2).  SPRY4-IT1  is derived from an intron within  SPRY4 , and is upregulated in melanoma cells; knockdown of its expression leads to cell growth arrest, invasion inhibition, and elevated rates of apoptosis. Upon depletion of EZH2 by RNA interference,  SPRY4-IT1  expression was restored, and transfection of  SPRY4-IT1  into NSCLC cells resulted in a significant antitumoral effect, both in culture and in xenografted nude mice. Moreover, overexpression of  SPRY4-IT1  was found to have a key role in the epithelial–mesenchymal transition through the regulation of E-cadherin and vimentin expression. In EZH2-knockdown cells, which characteristically showed impaired cell proliferation and metastasis, the induction of  SPRY4-IT1  depletion partially rescued the oncogenic phenotype, suggesting that  SPRY4-IT1  repression has an important role in EZH2 oncogenesis. Of most relevance, translation of these findings into human NSCLC tissue samples demonstrated that patients with low levels of  SPRY4-IT1  expression had a shorter overall survival time, suggesting that  SPRY4-IT1  could be a biomarker for poor prognosis of NSCLC.

cell death and disease

EZH2-mediated epigenetic suppression of long noncoding RNA SPRY4-IT1 promote s NSCLC cell proliferation and metastasis by affecting the epithelial–mesenchymal transition