Fig 2: Fascin-1 is prominently expressed and accumulates outside the lesion core after SCI. (A) Western blot analysis shows significant upregulation of Fascin-1 at 7 and 14 days after injury compared to the control (pre-operation, Pre). (B) Quantitative analysis of Fascin-1 expression in (A). The blots (n = 5 per group) were quantified by a densitometric method using ImageJ software. GAPDH was used as the loading control. The results are expressed as the mean ± SEM. ***p < 0.001 (14 days vs Pre); * p < 0.05 (7 days vs Pre); ##p < 0.01 (14 vs 3 days). (C) Double immunofluorescence labeling of spinal cord sagittal sections showing the spatiotemporal distribution of Fascin-1 (Red) and GFAP (Green) at Pre and 3, 7, and 14 days after injury. The asterisks indicate the lesion epicenter. Scale bar: 500 µm.

Fig 3: Snail mediates Rab25-induced fascin expression. (a) Cells were co-transfected with indicated vectors and siRNAs. Quantitative RT-PCR for fascin mRNA expression (mean±s.d. **P<0.01 versus control vector with scrambled siRNA, ###P<0.001 versus Rab25 overexpression with scrambled siRNA). (b) MCF-7 cells were co-transfected with indicated vectors and siRNAs. Immunoblotting. (c, d) Cells were co-transfected with indicated vectors and siRNAs (c), or stimulated with VEGF165aa (d). Immunofluorescence with an anti-fascin antibody. Original magnification, × 200; scale bar, 20 µm. (e) SKOV-3 cells were stimulated with VEGF165aa. ChIP analysis. (f) Correlation between FSCN1 gene expression and overall survival in breast (BC), ovarian (OC) and gastric (GC) cancer patients, P=0.01. The K–M plot was drawn in ‘kmplot.com’. (g) Correlation between FSCN1 and SANI1 gene expression in breast, ovarian and gastric cancer patients.

Fig 4: FSCN1 downregulates PTK6 expression in ESCC cell lines. (A–D) Lentivirus containing FSCN1 shRNA sequence (FSCN1-KD) and over-expressed sequence (FSCN1-OE) were added into ECA-109 and KYSE-150 mediums separately. Lentivirus expressing GFP only was used as a negative control (NC). The mRNA (A) and protein level (B–D) of FSCN1 in the 2 cell lines were detected. n = 3 per group, **p < 0.01, ***p < 0.001. (E–H) ECA-109 and KYSE-150 infected by NC, FSCN1-KD, and FSCN1-OE as indicated were harvested, and the mRNA (E) and protein level (F–H) of PTK6 in the 2 cell lines were detected. n = 3 per group, *p < 0.05, **p < 0.01, ***p < 0.001.

Fig 5: TAZ can promote the migration and accumulation of microglia around the lession core to form microglial scar after SCI and Fascin-1-TAZ pathway axis for positively regulating the migration of microglia. In this model, TAZ was downstream of Fascin-1 for regulating microglial migration. TAZ promoted the migration of microglia by Fascin-1 inducing TAZ nuclear accumulation of microglia, which contributed to the migration and accumulation of microglia around the lesion border to form microglial scars and promote functional recovery after SCI.