Conclusion
NR1D2 is shown to accelerate HCC progression via driving EMT.
Methods
We carried out PROGgeneV2 platform database analysis and compared NR1D2 expression in HCC tissues with that in adjacent noncancerous tissues by Western blotting. Cell proliferation, invasion, and migration were also assessed using a lentivirus system. Moreover, the relevant signalling proteins were evaluated.
Results
The PROGgeneV2 platform database analysis suggested an upregulated NR1D2 expression related to poor overall survival, or OS, in HCC, with higher levels in HCC, compared to the adjoining non-cancerous tissue. Depleting NR1D2 decreased HCC cell proliferation, migration and invasion in vitro, whilst in vivo downregulation revealed fewer metastatic nodules in the lungs. Furthermore, NR1D2 knockdown amplified epithelial marker, namely E-cadherin expressions, and decreased mesenchymal markers, ie, N-cadherin and vimentin expressions, with β-catenin overexpression.