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The interaction between LncRNA and RNA-binding protein (RBPs) plays an essential role in the regulation over the malignant progression of tumors. Previous studies on the mechanism of  SNHG1 , an emerging lncRNA, have primarily focused on the competing endogenous RNA (ceRNA) mechanism. Nevertheless, the underlying mechanism between  SNHG1  and RBPs in tumors remains to be explored, especially in prostate cancer (PCa).  SNHG1  expression profiles in PCa were determined through the analysis of TCGA data and tissue microarray at the RNA level. Gain- and loss-of-function experiments were performed to investigate the biological role of  SNHG1  in PCa initiation and progression. RNA-seq, immunoblotting, RNA pull-down and RNA immunoprecipitation analyses were utilized to clarify potential pathways with which  SNHG1  might be involved. Finally, rescue experiments were carried out to further confirm this mechanism. We found that  SNHG1  was dominantly expressed in the nuclei of PCa cells and significantly upregulated in PCa patients. The higher expression level of  SNHG1  was dramatically correlated with tumor metastasis and patient survival. Functionally, overexpression of  SNHG1  in PCa cells induced epithelial–mesenchymal transition (EMT), accompanied by down-regulation of the epithelial marker,  E-cadherin , and up-regulation of the mesenchymal marker,  vimentin . Increased proliferation and migration, as well as accelerated xenograft tumor growth, were observed in  SNHG1 -overexpressing PCa cells, while opposite effects were achieved in  SNHG1 -silenced cells. Mechanistically,  SNHG1  competitively interacted with  hnRNPL  to impair the translation of protein  E-cadherin , thus activating the effect of  SNHG1  on the EMT pathway, eventually promoting the metastasis of PCa. Our findings demonstrate that  SNHG1  is a positive regulator of EMT activation through the  SNHG1 - hnRNPL -CDH1 axis.  SNHG1  may serve as a novel potential therapeutic target for PCa.

LncRNA SNHG1 and RNA binding protein hnRNPL form a complex and coregulate CDH1 to boost the growth and metastasis of prostate cancer