Fig. 6: NURR1 can promote in vitro migration and invasion potential of prostate cancer cells.

A, B Wound healing assay. Left: Representative images of scratched and recovered wound areas (demarcated by dotted lines) on confluence monolayers of infectants of NURR1, shNURR1 and their controls taken at 0- and 48-h time points. Right: Semi-quantitative analysis of wound closure. Results showed that LNCaP-NURR1 and DU 145-NURR1 infectants exhibited significant higher migration potential, whereas DU 145-shNURR1 and PC-3-shNURR1 infectants displayed slower migration potential as compared to their corresponding controls. C, D Transwell-invasion assay. Left: Representative images of invaded cells. Right: Quantification analysis of field area occupied by invaded cells (% of total field area). Results showed that LNCaP-NURR1 and DU 145-NURR1 infectants manifested significant higher invasion potential, whereas DU 145-shNURR1 and PC-3-shNURR1 infectants showed lower invasion potential as compared to their control infectants. E, F Immunoblot analysis of EMT markers in NURR1- and shNURR1 infectants. Results showed that LNCaP-NURR1 and VCaP-NURR1 infectants expressed enhanced levels of EMT markers (increased vimentin and N-cadherin levels, suppressed E-cadherin level), whereas PC-3-shNURR1 and DU 145-shNURR1 infectants displayed the reversed profile of these markers (reduced vimentin, snail1, twist and MMP9 levels; increased ZO-1 level). G Immunoblot analysis of EMT markers in DU 145-NURR1 infectants treated with C-DIM-12/IWP-2 or plus CTNNB1 knockout. Results showed that treatment with C-DIM-12 or IWP-2 induced significant loss of epithelial cell marker ZO-1 expression and comparable high level of MMP9 as in untreated DU 145-NURR1 infectants. Knockout of CTNNB1 could attenuate the expression levels of MMP9 and ZO-1 in DU 145-NURR1 infectants. *P < 0.05; **P < 0.01 versus vector or scramble controls.